30 must-read documents calculated according to the "heart-warming factor" in August 2021.
500 Divine Journal Review: Intermittent Fasting and Cancer Prevention
CA-A Cancer Journal for Clinicians——[508.702]
① Calorie restriction can reduce the risk of obesity-related cancers by controlling weight, but intermittently The research results of sexual fasting (IF) in animal models are controversial, and it may even be harmful in some tumor models (or related to IF mode); ② Animal studies have shown that IF may reduce IGF-1 and promote Ketone body is produced and autophagy can improve cancer, but the status of these mechanisms in humans has yet to be verified; ③Due to the lack of high-quality clinical trials, the impact of IF on the incidence and prognosis of human cancer is still unknown. Preliminary studies have shown that In some cancer patients, prolonging fasting time is safe and may reduce chemotherapy-related toxicity and tumor growth; ④ It is not recommended that cancer patients undergoing treatment receive IF outside of clinical trials, but want to reduce cancer risk through weight management Of adults can consider incorporating IF into a healthy lifestyle.
[Editor-in-chief's comment]
Calorie restriction is a fasting method that can reduce the risk of cancer in laboratory animals and humans, but it is difficult to adhere to for a long time. Intermittent fasting (IF) is another fasting method that has been studied in recent years, but the research on IF and cancer is still in its infancy. CA: A Cancer Journal for Clinicians recently published a long review article, focusing on the basic and clinical research progress of IF in cancer prevention and treatment, discussing the current knowledge gaps (especially in terms of clinical evidence), and providing clinicians with Recommendations based on current research evidence,Recommended for professionals. (@Mildbreeze)
[Original information]
Intermittent fasting in the prevention and treatment of cancer
2021-08-12, doi: 10.3322/caac.21694
Peking University team NEJM: potassium Span10span replaces some sodium salts, which can reduce the risk of cardiovascular events and premature death
New England Journal of Medicine——[91.245]
① An unblinded, cluster randomized trial involving 20,995 patients with stroke in 600 villages in China Patients with history or hypertension patients ≥60 years old were randomly divided into the intervention group (75% sodium + 25% potassium) and the control group (total sodium) based on the village as a unit of 1:1, with an average follow-up of 4.74 Years; ② Compared with the control group, the incidence of stroke, major cardiovascular events and all-cause death in the intervention group were significantly reduced, with RRs of 0.86, 0.87 and 0.88, respectively; ③ In terms of safety, hyperkalemia There was no significant difference between the two groups in the incidence rate.
[Editor-in-chief's comment]
Salt replacement interventions that reduce sodium and increase potassium have been shown to lower blood pressure, but the impact on cardiovascular outcomes and their safety are uncertain. Peking University Wu Yangfeng, Tian Maoyi and their team recently published a randomized controlled study in the New England Journal of Medicine, involving 20,995 subjects in 600 villages in my country, exploring salt substitutes (containing 25% potassium) compared to conventional The risks and benefits of salt (full sodium salt) in terms of stroke, cardiovascular events, death and hyperkalemia.The results show that in people who have a history of stroke or who are over 60 years old and have hypertension, the use of salt substitutes can significantly reduce stroke, major cardiovascular events and mortality, and is safe. (@Mildbreeze)
[Original Information]
Effect of Salt Substitution on Cardiovascular Events and Death
2021-08-29, doi: 10.1056/NEJMoa2105675
SpanNEJ Senior Citizen: Team Weili Cai Blood pressure patients must strengthen their blood pressure!
New England Journal of Medicine——[91.245]
① In a multicenter randomized controlled trial, 8511 Chinese hypertension patients aged 60-80 were divided into the intensive treatment group and the standard treatment group, with a scale of 110~<130> systolic blood pressure of the two groups after 1 year were 127.5 and 135.3 mmHg; ③ During the median follow-up period of 3.34 years, the two groups had 3.5% and 4.6% respectively The risk of multiple cardiovascular events in patients with the intensive treatment group was significantly reduced by 26%. Among them, the risks of stroke, acute coronary syndrome and acute decompensated heart failure were reduced by 33%, 33% and 73%; ④ Safety and There was no significant difference in renal outcome between the two groups, but the incidence of hypotension increased in the intensive treatment group.
[Editor-in-chief's comment]
Hypertension is a common risk factor for cardiovascular death, but there is no unified recommendation for blood pressure management goals for elderly hypertensive patients given by different guidelines. New England Journal of Medicine recently published a large-scale multi-center clinical trial (STEP trial) carried out by Cai Jun, Zhang Weili and their team from the Hypertension Center of Fuwai Hospital.The results show that for elderly hypertensive patients, compared with standard treatment (130 to <150>
[Original information]
Trial of Intensive Blood-Pressure Control in Older Patients with Hypertension
2021-08-30, doi: 10.1056/NEJMoa2111437
Nature: How to transform the high fructose diet "The intestine promotes obesity?
Nature——[49.962]
① In mice, dietary fructose can promote the survival of small intestinal epithelial cells, cause intestinal villi to grow, increase the intestinal surface area and enhance the absorption of lipids, thereby increasing high fat Diet-induced obesity; ② fructose is converted into fructose-1-phosphate (F1P) by hexulose kinase (KHK) after entering intestinal cells, F1P can inhibit the activity of pyruvate kinase M2 isoform (PKM2) (The high-activity PKM2 tetramer is broken down into low-activity monomers), and then by up-regulating HIF-1α to enhance the viability of intestinal cells and colon cancer cells under hypoxia; ③ knock out KHK or use The drug TEPP-46 activates PKM2, which can inhibit the growth of intestinal villi, increased lipid absorption and intestinal tumor growth in mice caused by high fructose corn syrup.
[Editor-in-Chief’s comment]
Excessive dietary fructose intake is associated with an increase in obesity and cancer.But the relevant mechanism still needs to be explained in depth. A study recently published by Nature found that a high-fructose diet can enhance the survival ability of mouse intestinal epithelial cells in the hypoxic environment of the intestinal lumen, resulting in an increase in the length of intestinal villi, an increase in intestinal surface area, an increase in lipid absorption, and promotion The growth and obesity of intestinal tumor were analyzed, and the molecular mechanism behind it was revealed. These findings may explain the effect of fructose in breast milk on the growth of infants and the reason why a western-style diet with a large amount of fructose sweeteners aggravates obesity. (@Mildbreeze)
[Original information]
Dietary fructose improves intestinal cell survival and nutrient absorption
2021-08-18, doi: 10.1038/s41586-021-03827-2
Nature: How to use bacteria "Upper" dead intestinal cells?
Nature——[49.962]
① Salmonella and other Enterobacteriaceae bacteria can use the nutrients released by apoptotic intestinal cells to promote their own growth and colonization in the mouse intestine; ② These nutrients are soluble small molecules/metabolites of <3kda,> pyruvate and metabolites that depend on the release of membrane channel Panx1; ③Mechanistically, these components can induce the transcriptional response of Salmonella and up-regulate the encoding pyruvate. The expression of pflB gene of formate lyase drives the growth and colonization of Salmonella; ④ Intestinal epithelial cell apoptosis can make mice susceptible to exogenous Salmonella infection, and can also promote the overgrowth of endogenous Enterobacteriaceae bacteria.
[Editor-in-chief's comment] A new study published by
Nature reveals a new mechanism of host-bacterial interaction.The study demonstrated through a variety of cell lines and mouse model experiments that Enterobacteriaceae bacteria (including pathogenic bacteria, symbiotic bacteria and conditional pathogenic bacteria) can use the nutrients released by apoptotic intestinal epithelial cells to promote themselves Grow, thereby establishing a colonization advantage in the host intestine. In intestinal diseases such as food-borne infections, inflammatory bowel disease, and chemotherapy-induced intestinal mucositis, bacterial infection and inflammation can cause intestinal epithelial cell apoptosis, which in turn increases the body’s exogenous intestinal induced The susceptibility of pathogens also provides "fuel" for the excessive proliferation of enterobacteriaceae that originally colonized the intestines, thereby promoting disease-related flora imbalance. (@Mildbreeze)
[Original information]
Microbes exploit death-induced nutrient release by gut epithelial cells
2021-08-04, doi: 10.1038/s41586-021-03785-9
Nature Loneliness changes the state of the brain, leading to sleep less and eat more
Nature——[49.962]
① Long-term (7 days) and short-term (1 day) social isolation causes different behaviors and brain states of fruit flies The former will reduce sleep and eat more in fruit flies; ② Long-term loneliness changes the expression of metabolic genes in the brain of fruit flies, accompanied by changes in gene expression related to hunger and appetite. These changes cause the brain to send out hunger signals, leading to Increased eating; ③Mechanistically, long-term loneliness can cause sleep and eating problems by activating P2 neurons. Inhibition of this neuron can reduce sleep and eating disorders caused by long-term loneliness, while activation of this neuron can lead to short-term social isolation in fruit flies. Loneliness-related phenotypes.
[Editor-in-chief comment]
Social isolation and loneliness have a major impact on public health.A newly published study by Nature, through quantitative analysis of the behavior and brain transcriptome of fruit flies, found that the brain state of fruit flies that lived alone for a long time changed, leading to reduced sleep and increased eating, and identified the mediating role. Of neurons. These findings have brought new enlightenment to the interpretation of the biological mechanism of long-term loneliness causing health problems such as sleep, diet, and metabolism. (@Mildbreeze)
[Original information]
Chronic social isolation signals starvation and reduces sleep in Drosophila
2021-08-18, doi: 10.1038/s41586-021-03837-0
Science: High fat Diet promotes the new mechanism of intestinal microbes producing TMA
Science——[47.728]
① Experiments in mice show that high-fat diet can cause inflammation of the intestinal mucosa and lead to a decrease in the activity of epithelial cells and mitochondria . Causes an increase in the electron receptors (oxygen and nitrate) in the respiratory chain, and the above effects do not depend on the intestinal flora; ② The increase in oxygen and nitrate provides a growth advantage for Escherichia coli and promotes its cutC gene ( Participate in the conversion of choline to TMA) expression to help it use choline as a carbon source for growth; ③ The enhancement of the catabolism of choline by E. coli will lead to an increase in the level of TMAO in the blood of mice; ④ The use of drugs to improve mitochondria Activity, can reduce TMAO levels in mice on a high-fat diet.
[Editor-in-chief's comment]
Western dietary patterns increase the risk of cardiovascular disease. Previous studies have shown that this diet will promote the production of choline,Choline is further metabolized by the intestinal flora into trimethylamine (TMA), and then converted into trimethylamine oxide (TMAO) in the liver, and TMAO is closely related to cardiovascular disease. Science recently published a collaborative study between the Vanderbilt Medical University Center and the University of California, Davis team, revealing a new mechanism by which a high-fat diet promotes the production of TMAO through intestinal flora, namely high-fat diet_ span10span will change the physiological state of the host's intestinal epithelial cells, thereby affecting the intestinal environment, promoting the catabolism of choline by E. coli, and ultimately leading to an increase in the level of TMAO in the blood. This research suggests that there is a complex interaction between our diet, intestinal physiology, and intestinal flora, and it also reminds us of the importance of a healthy diet. (@ Hard Research 617(ꈍᴗꈍ))
[Original information]
High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide
2021-08-13, doi: 10.1126/science. aba3683
Science: How does specific enterococcus enhance cancer immunotherapy?
Science——[47.728]
① Specific Enterococcus bacteria (such as Enterococcus faecium) can improve the response of tumor mice to anti-PD-L1 immune checkpoint inhibitor (ICI) treatment; ② these Enterococcus expresses and secretes homologues of the peptidoglycan hydrolase SagA, which can reconstruct the components of the bacterial wall peptidoglycan to generate immunologically active wall peptides (such as muramyl dipeptide MDP), thereby passing Activate NOD2 signal to enhance the effect of immunotherapy; ③ Orally supplement model mice with engineered bacteria expressing SagA (such as , Enterococcus faecalis and probiotics expressing SagA) or injection of synthetic MDP,Both can enhance the anti-tumor efficacy of ICI (including anti-CTLA-4).
[Editor-in-chief's comment]
Intestinal flora can affect the effect of PD-L1 immunotherapy for cancer patients, but the relevant mechanisms have yet to be explored. A study recently published by Science found that some bacteria of the genus Enterococcus can enhance the efficacy of anti-PD-L1 immunotherapy on model mice. Mechanistically, these enterococci can secrete an enzyme called SagA, which can degrade the peptidoglycan component of the bacterial wall, thereby releasing cell wall peptide fragments that can activate the pattern recognition receptor NOD2, and improve the immunotherapy response. Researchers believe that bacterial peptidoglycan remodeling and the production of immunologically active small molecules may be a type of mechanism to enhance the efficacy of immunotherapy, or have broad clinical application prospects in cancer immunotherapy and prognosis prediction. (@Mildbreeze)
[Original information]
Enterococcus peptidoglycan remodeling promotes checkpoint inhibitor cancer immunotherapy
2021-08-27, doi: 10.1126/science.abc9113
How does science affect the maternal intestinal infection during pregnancy
Immunity?
Science——[47.728]
① Transient infection of pregnant mice with Yersinia pseudotuberculosis (YopM), the offspring of the mice will have an increase in the number of intestinal-specific Th17 cells and increased responsiveness to the flora ② This long-term effect on the offspring’s intestinal immunity does not depend on the maternal flora, but is mediated in the uterus by the pro-inflammatory cytokine IL-6: infection increases maternal IL-6, and IL-6 acts on Fetal intestinal epithelial stem cells increase their chromatin openness and change downstream cell functions (such as increasing the expression of antigen presentation molecules and antimicrobial peptide); ③ pregnant mice infected with YopM or injected IL-6,It can increase the resistance of its offspring to intestinal pathogenic bacteria infection, but at the same time, it is also more susceptible to intestinal inflammation.
[Editor-in-Chief's comment]
Most infections that occur during pregnancy are mild and short-lived, but it is still unclear whether this infection will have a long-term impact on the immune system of offspring. A new study published by Science shows that infections from the mother during pregnancy can have a continuous tissue-specific effect on the immune function of the offspring. The study found that the transient infection of pregnant mice with common food-borne pathogens can cause the level of the pro-inflammatory cytokine IL-6 to increase. IL-6 can directly act on the fetal rat intestinal epithelial stem cells in the uterus to change its epigenetic memory, thereby causing a lasting impact on the intestinal immune homeostasis of the offspring. These findings reveal a new mechanism by which maternal microbial exposure affects the immune development of offspring and are recommended for professional reference. (@Mildbreeze)
[Original information]
Prenatal maternal infection promotes tissue-specific immunity and inflammation in offspring
2021-08-27, doi: 10.1126/science.abf3002
Science: Human Lifetime Metabolism Level 4 stages of change
Science——[47.728]
① Include 6421 people from 29 countries and analyze the daily energy consumption of humans from 8 days old to 95 years old; ② Total energy consumption increases with lean body weight Shows a power-law increase. After adjusting for fat-free weight, it is found that there are 4 different stages in the change of daily energy consumption (total energy consumption and basic energy consumption) (0-1 years old, 1-20 years old, 20-60 years old, >60 years old) ③ The energy consumption level of newborns is similar to that of adults. The energy consumption level from birth to 1 year of age rises rapidly to 150% of adulthood, and then continues to decline and remains stable during the period of 20-60 years.After 60 years of age, it began to slowly decrease again; ④ The modeling analysis showed that the tissue metabolic rate at different stages followed the corrected trajectory of basic energy consumption.
[Editor-in-chief's comment]
The metabolic rate (rate of energy consumption) of a person is not static during a lifetime. It is generally believed that the human body’s metabolic rate is highest during adolescence and gradually decreases after adulthood. Phenomenon such as "half-and-a-half son, eat to death" and "middle-aged to be blessed" seem to be good proofs. However, a study recently published by Science, through the analysis of the daily energy consumption of the human body throughout the life cycle, found that the metabolic level of a person's lifetime reaches its peak at 1 year old, and then steadily decreases until 20.5 years old, and maintains it for the next 40 years. Stablize. These results suggest that the tissue metabolism level of the human body is not constant, but there are physiologically significant changes in different life stages. For example, the high metabolic level in the early life may be related to the vigorous growth and development of the body, while the reduced energy consumption in old age It may reflect the "slowing down" of cells, tissues and organs. (@Mildbreeze)
[Original information]
Daily energy expenditure through the human life course
2021-08-13, doi: 10.1126/science.abe5017
Cell: ILC3 dysregulation promotes colorectal cancer development and immunity Therapeutic resistance
Cell——[41.582]
① In the CRC tumor microenvironment of humans and mice, ILC3 changes, that is, the number is reduced, the plasticity is enhanced (transition to ILC1), and the balance with T cells is abnormal These changes are similar to those in IBD ; ② Normally, ILC3 and T cells interact through the antigen-presenting molecule MHCII, shaping the intestinal flora to induce type 1 immunity; ③ Specific in mouse ILC3 Knock out MHCII,It will weaken intestinal type 1 immunity, promote the development of aggressive CRC and resist anti-PD-1 immunotherapy; ④ The intestinal flora of patients with IBD changes (especially Bacteroides), transplanting its flora to mice will weaken the intestine 1 Type immunity and response to immunotherapy.
[Editor-in-Chief comment]
Type 3 natural lymphocytes (ILC3) can regulate intestinal flora, immunity and inflammation, but their role in colorectal cancer (CRC) is not yet clear. A new study published by Cell found that ILC3 has similar changes to inflammatory bowel disease (IBD) in the CRC tumor microenvironment. Mouse experiments further revealed that ILC3 interacts with T cells to shape the intestinal flora and promote type 1 immune response, thereby inhibiting CRC (especially IBD-related CRC) tumor progression and promoting the response to immunotherapy. These findings suggest that ILC3 dysfunction and the imbalance of its interaction with T cells may play a key role in IBD and CRC, and provide new ideas for further research on intervention and treatment of these two diseases. (@Mildbreeze)
[Original information]
Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer
2021-08-17, doi: 10.1016/j.cell.2021.07.029
h113 Cell. Multicellular immune center in colorectal cancer
Cell——[41.582]
① Include 28 patients who can perform mismatch repair (MMRp) and 34 patients with mismatch repair defect (MMRd), for colorectal tumors Perform single-cell sequencing with 371,223 cells in adjacent normal tissues; ②Identified 88 cell subgroups and 204 related gene expression programs,The monocytes and macrophages at the tumor site are remodeled, and more immune activation programs are expressed in MMRd tumors; ③ The expression programs of different cell types are determined, and these expression programs are in the affected individuals. Common changes in tumors; ④ There is a bone marrow cell attraction center at the tumor-lumen interface, and an immune center enriched with MMRd, which is composed of T cells and cells expressing CXCR3 ligand.
[Editor-in-Chief's comment]
The immune response of cancer is highly variable, and mismatch repair defective (MMRd) tumors exhibit more anti-tumor immunity than tumors capable of performing mismatch repair (MMRp). The article published by Cell yesterday developed a systematic method based on single-cell RNA sequencing (scRNA-seq) profiling to discover cell types, their potential gene expression programs and cell communities, and used this method to study human MMRd and Features of MMRp CRC. A bone marrow cell attraction center related to tissue damage and an MMRd-enriched immune center in the tumor were found at the tumor-lumen interface. The center is composed of activated T cells, cells expressing CXCR3 ligand, and malignant myeloid cells . This research reveals the potential mechanism of interaction between spatial tissue immune and malignant cell network by identifying the cellular programs that interact. (@Nana)
[Original information]
Spatially organized multicellular immune hubs in human colorectal cancer
2021-08-27, doi: 10.1016/j.cell.2021.08.003
Nature Reviews: a picture Understand how oral bacteria can worsen enteritis
Nature Reviews Gastroenterology and Hepatology——[46.802]
① The colonization of oral bacteria in the intestine is limited in a healthy state,However, in IBD, specific oral bacteria (such as , Klebsiella pneumoniae, Fusobacterium nucleatum, etc.) migrate and accumulate in the intestinal tract; ② Inflammation of the oral cavity and intestinal tract have in common: pathogenic bacteria Invasion of epithelial tissues, triggering inflammatory reactions such as Th17 response, and the production of nitric oxide and tissue destruction caused by inflammation in turn aggravate the imbalance of flora and the expansion of pathogenic bacteria; ③ Oral bacteria in IBD have three stages of intestinal expansion: 1) Disease-related bacteria in the oral cavity increase + the colonization resistance of the intestine is weakened, 2) oral bacteria migrate to the intestine, 3) oral bacteria colonize the intestine and worsen IBD.
[Editor-in-chief's comment]
Periodontitis is a common oral inflammation. Recent studies have shown that there is a disorder of oral flora in periodontitis and is associated with inflammatory bowel disease (IBD). A recent opinion review article published by Nature Reviews Gastroenterology and Hepatology believes that in IBD, oral disease-related bacteria can translocate and colonize the intestine, thereby directly exacerbating intestinal inflammation, and proposed a three-stage model to illustrate this process The pathological mechanism emphasizes the role of the interaction between pathogenic bacteria and immune inflammation, which has guiding significance for the study of prevention and treatment methods for diseases such as IBD. This article once again reminded the importance of oral health, "disease comes from the mouth", intestinal health must not ignore the oral cavity. We specially compiled the pictures in the article into a picture to understand, hoping to help you increase your knowledge. (@Mildbreeze)
[Original information]
The role of oral bacteria in inflammatory bowel disease
2021-08-16, doi: 10.1038/s41575-021-00488-4
BMJ: Low GI/ GL diet helps to improve diabetes,How's the effect?
British Medical Journal——[39.89]
① Include 29 randomized controlled trials (1617 patients with type 1 and type 2 diabetes with acceptable disease control) to assess low glycemic index (GI)/glycemic load (GL) diet intervention (≥3 months) on the blood glucose and cardiovascular risk indicators of diabetes; ② Compared with the control diet, the low GI/GL diet significantly reduced glycosylated hemoglobin (HbA1c) (the difference was -0.31 %), fasting blood glucose, LDL-C, non-HDL-C, apolipoprotein B, triglycerides, body weight, BMI and CRP (inflammation markers), but does not improve blood insulin, HDL-C, waist circumference, blood pressure Significant; ③ The evidence that low GI/GL diet improves HbA1c is highly certain.
[Editor-in-chief's comment]
The latest study published by British Medical Journal included 29 randomized controlled trials, using systematic reviews and meta-analysis methods to quantitatively assess low glycemic index (GI)/glycemic load (GL) The impact of dietary intervention on diabetes shows that low GI/GL diet can cause small and meaningful improvements in blood glucose control, blood lipids, obesity and inflammation. This study supports the beneficial effects of this dietary supplementary intervention on people with diabetes. (@Mildbreeze)
[Original information]
Effect of low glycaemic index or load dietary patterns on glycaemic control and cardiometabolic risk factors in diabetes: systematic review and meta-analysis of randomised controlled trials
2021-08-05 , doi: 10.1136/bmj.n1651
How do bacteria promote the occurrence of various cancers? (Review)
Cancer Discovery——[39.397]
① The mechanism of bacterial cancer promotion: the damaging effect of bacterial toxins on DNA,Bacteria caused by Western diet produce harmful metabolites, inflammation caused by interaction with host cells, chronic infection and the formation of aggressive biofilms, inhibit the body's anti-tumor immune response; ② Hypothesis that bacteria are involved in tumorigenesis: one or a group of tumors The driver-passenger model of bacterial recruitment or coordination with other microorganisms to promote tumorigenesis, the key hypothesis model that a single tumorigenic bacteria is sufficient to promote carcinogenesis, the hit-and-run model of tumorigenesis caused by the temporary colonization of tumorigenic bacteria, etc.; ③ Koch's law The application of , such as Helicobacter pylori, promotes the occurrence of gastric cancer in accordance with Koch's law.
[Editor-in-chief's comment]
Cancer Discovery published a review that discussed the possible mechanisms of bacteria in promoting cancer, and emphasized many types of cancers, including gastrointestinal and non-intestinal cancers, development and microbiome Relationship. Research on the cancer microbiome is helpful to understand the various mechanisms by which the microbiota affects the occurrence and development of cancer, and provides reference ideas for cancer prevention and treatment. (@Nana)
[Original information]
The Cancer Microbiome: Recent Highlights and Knowledge Gaps
2021-08-16, doi: 10.1158/2159-8290.CD-21-0324
Yu Jun team : A high-fat diet makes intestinal bacteria and metabolites "corrupted" to promote colorectal cancer
Gastroenterology——[22.682]
① In two mouse models of colorectal cancer (CRC), high-fat diet (HFD) Both can promote the development of CRC, and this effect depends on the intestinal flora; ② In mechanism, HFD drives CRC by changing the composition of the flora and metabolites, and damaging the intestinal barrier function; ③ Including the enrichment of 2 potential pathogens of Alipipes Bacteria, reduce the beneficial Parabacteroides dienii, increase the harmful metabolites LPA, reduce the beneficial metabolites NDGA and nervonic acid,These bacteria and metabolites can affect CRC cell proliferation and/or cell connection; ④ Only transplantation of HFD mouse feces (containing flora and metabolites) can promote colonic cell proliferation and cancer-promoting gene expression in sterile mice, and damage the intestines. Barrier function.
[Editor's comment]
A high-fat diet increases the risk of colorectal cancer. Gastroenterology recently published research results from Yu Jun’s team at the Chinese University of Hong Kong. It found that high-fat diet can drive colorectal tumors by inducing intestinal flora imbalance, metabolic changes and intestinal epithelial barrier dysfunction in mice, and revealed that there are Potentially critical bacteria and metabolites. These findings provide new ideas for targeting the intestinal flora and its metabolites to prevent and treat colorectal cancer related to high-fat diet. (@Mildbreeze)
[Original information]
High-Fat Diet Promotes Colorectal Tumorigenesis through Modulating Gut Microbiota and Metabolites
2021-08-26, doi: 10.1053/j.gastro.2021.0hr
Jun + Huang Weishen + Xia Qiang: Changes in metabolites entering the liver from the intestines or involved in the occurrence of liver cancerGut——[23.059]
① Serum of 52 liver cancer (HCC) patients and 50 healthy people (portal and central) Intravenous), liver tissue, and stool samples were screened for differential metabolites, and another 100 people lined up (50 HCC patients and 50 controls) for verification; ② Differences in serum, liver tissue, and fecal metabolites between HCC patients and control individuals Obviously; ③ The portal vein serum and liver tissue of HCC patients have higher levels of DL-3-phenyllactic acid, L-tryptophan, glycocholic acid and 1-methylnicotinamide, which are associated with impaired liver function and poor survival The rate is related; ④ HCC patients have lower levels of linoleic acid and phenol in the portal vein and feces,Both can significantly inhibit the proliferation of HCC cells.
[Editor-in-Chief comment]
Metabolite changes play an important role in the tumorigenesis of hepatocellular carcinoma (HCC). Yu Jun, Huang Weishen from the Chinese University of Hong Kong, and Xia Qiang from Shanghai Jiaotong University and their team published an article on Gut. Through comprehensive metabolomics analysis of the changes in portal vein blood metabolites of HCC patients and healthy controls in two cohorts, and The changes in metabolites in liver tissue and stool samples were compared. The results showed that the metabolome of patients with HCC has changed, especially the changes of metabolites in the portal vein, suggesting that some metabolites may play a role in the occurrence of HCC. (@爱的择选)
[Original information]
Integrative metabolomic characterisation identifies altered portal vein serum metabolome contributing to human hepatocellular carcinoma
2021-08-03, doi: 10.1136/gutjnl-2021-32518912
Domestic team Cell Sub-Journal: Supplementing selenium inhibits Th1 differentiation, or can alleviate Crohn’s diseaseImmunity——[31.745]
① The results of single-cell sequencing and metabolome analysis show that Th1-like cells in patients with Crohn’s disease Subpopulations are enriched, and the selenium level is significantly reduced; ② IBD specific metabolites affect the differentiation mode of T cells, especially selenium can significantly affect the differentiation of Th1 cells; ③ Mechanism, selenium can promote the purine synthesis salvage pathway of Th1 cells, In order to enhance selenoprotein W (SELW)-mediated intracellular reactive oxygen removal, and promote SELW-dependent serine hydroxymethyltransferase 2 (SHMT2) degradation to inhibit one-carbon metabolism, thereby inhibiting Th1 differentiation; ④ in In mouse models of colitis and Crohn’s disease patients,Supplementing selenite can relieve colitis.
[Editor-in-chief's comment]
Jin Jin's team from Zhejiang University and Cao Qian's team from Run Run Run Shaw Hospital, Zhejiang University School of Medicine published a new study on Immunity and found that Th1 in the colon of patients with Crohn's disease The cells are enriched, and the selenium level is significantly reduced. In terms of mechanism, selenium can inhibit the differentiation of Th1 cells by promoting the salvage pathway of purine synthesis and inhibiting one-carbon metabolism. In mouse models of colitis and Crohn’s disease, supplementation with selenite can alleviate colitis. (@Szx)
[Original information]
Multiomics analyses reveal a critical role of selenium in controlling T cell differentiation in Crohn's disease
2021-08-02, doi: 10.1016/j.immuni.2021.07.004
Domestic team: Changes in the intestinal flora of children with autism
Gut——[23.059]
① Include 72 children with ASD and 74 children with normal development, and perform deep metagenomic sequencing on stool samples; ② ASD and actual age have the most significant impact on children's fecal flora, but diet has no correlation; ③Compared with normal developing children, the composition of fecal flora of children with ASD has changed significantly, and the bacterial abundance is significantly increased; ④ 5 This bacterial species can distinguish children with ASD from children with normal development (AUC=76.2% in the verification cohort); ⑤ The function of the flora related to neurotransmitter biosynthesis is significantly reduced in children with ASD; ⑥ The difference observed in children with normal development The developmental dynamics of growth-related intestinal bacteria disappear throughout the early life of children with ASD.
[Editor-in-chief's comment]
A new study published on Gut by Huang Xiujuan's team from the Chinese University of Hong Kong and Ruth Chan's team from Hong Kong Polytechnic University,The differences in intestinal flora between children with autism spectrum disorder (ASD) and children with normal development were compared. (@Szx)
[Original information]
Underdevelopment of the gut microbiota and bacteria species as non-invasive markers of prediction in children with autism spectrum disorder
2021-07-26, doi: 10.1136/gutjnl-2020 -324015
Cell: A new anti-inflammatory mechanism of bacterial bile acid metabolites
Cell Host and Microbe——[21.023]
① The bile acid metabolite isoalloLCA promotes the open chromatin structure of the Foxp3 promoter region Formation of anti-inflammatory Treg; ② Bacteroides bacteria can use intestinal bacterial metabolite 3-oxoLCA to produce isoalloLCA, and contain isoalloLCA gene cluster; ③ Nuclear hormone receptor NR4A1 is necessary for isoalloLCA to enhance Treg differentiation ④ In patients with inflammatory bowel disease, the levels of isoalloLCA and its related biosynthetic genes are significantly reduced, that is, isoalloLCA and isoalloLCA-producing bacteria may play an important role in maintaining the body's immune homeostasis.
[Editor-in-chief's comment]
Cell Host and Microbe recently published an article that found that Bacteroides bacteria can convert the secondary bile acid 3-oxoLCA into isoalloLCA, isoalloLCA enhances the differentiation of Treg cells through the nuclear hormone receptor NR4A1, It suggests that symbiotic bacteria participate in the formation of immune tolerance homeostasis.(@爱的择择)
[Original information]
A bacterial bile acid metabolite modulates Treg activity through the nuclear hormone receptor NR4A1
2021-08-19, doi: 10.1016/j.chom.2021.07.013
Mining enzymes in human intestinal flora based on omics data (review)
Trends in Biotechnology——[19.536]
① Omics data combined with bioinformatics methods can be used to predict enzymes in human intestinal flora ② Method for mining enzymes based on metabolites: Combine transcriptome and metatranscriptome data, compare genomic data, and analyze the correlation between metagenomic-metabonomics data; ③ Method based on sequence annotation enzyme function: Based on common biochemical characteristics, Protein sequence similarity network analysis and genome background analysis; ④ Method for annotating enzyme functions based on protein structure: protein structure classification, high-throughput molecular docking; ⑤ The mining of intestinal flora-related enzymes is helpful to analyze the catalysis and mechanism of the flora , Or can guide the application of intestinal flora in clinical diagnosis and treatment.
[Editor-in-chief's comment]
The intestinal flora can express a large number of enzymes with different functions, mediate the production of flora metabolites, thereby affecting the physiology and health of the host, but there are still a lot of gaps in the research on these enzymes. . Trends in Biotechnology recently published a review, which summarized in detail the research methods for mining enzymes in the intestinal flora based on omics data (metagenomics, metabonomics, transcriptomes, macrotranscriptomes, etc.), which is recommended for professionals to refer to. (@Mildbreeze)
[Original information]
Discovery and mining of enzymes from the human gut microbiome
2021-07-22, doi: 10.1016/j.tibtech.2021.06.008
Zhang Hongfu +Yin Jie: How does the intestinal flora regulate appetite (review)
Microbiome——[14.65]
① The physiological control of appetite is produced by peripheral organs to promote and suppress appetite hormones (such as leptin, ghrelin, Insulin, etc.) mediated,Intestinal flora can affect the composition and function of these hormones; ② Intestinal flora metabolites and components (SCFA, succinic acid, tryptophan metabolites, GABA, BCAA, bile acid, etc.) can regulate hormone secretion and immune system And directly act on hypothalamic neurons to affect appetite; ③ Intestinal flora protein ClpB can be used as an α-melanocyte stimulating hormone mimic, which can inhibit appetite through direct or indirect mechanisms; ④ Regulate intestinal flora to improve appetite It has clinical application potential in related diseases.
[Editor-in-chief's comment]
Zhang Hongfu, Chen Liang, Chinese Academy of Agricultural Sciences, and Yin Jie, Hunan Agricultural University, and their team recently published a review in Microbiome, introducing the regulation of intestinal flora (especially its metabolites) on host appetite The role and mechanism, and prospects for its clinical application, it is recommended for professionals to pay attention. (@Mildbreeze)
[Original information]
From gut microbiota to host appetite: gut microbiota-derived metabolites as key regulators
2021-07-20, doi: 10.1186/s40168-021-01093-y _p2hr
Chen Congying + Academician Huang Lusheng: Intestinal flora affects pig fat accumulation
Microbiome——[14.65]
① The abundance of Prevotella copri is significantly positively correlated with pig fat accumulation; ② The abundance of P. copri increases High is significantly related to the increase in the concentration of obesity-related metabolites (LPS, branched chain amino acids, aromatic amino acids, metabolites of arachidonic acid, etc.) in pig serum; ③ In sterile mice, colonized and isolated from pigs P. copri can increase fat accumulation; ④ In mechanism, the colonization of P. copri can activate the chronic inflammatory response in mice through TLR4 and mTOR signaling pathways.And significantly up-regulate the expression of genes related to fat formation and fat accumulation, while inhibiting the expression of genes related to lipolysis, fat transport and muscle growth.
[Editor-in-chief's comment]
Academician Chen Congying and Huang Lusheng from Jiangxi Agricultural University and the research team published a new research result on Microbiome, found and verified in 698 commercial pigs (Duroc pigs), pigs The abundance of Prevotella copri in the intestinal flora is positively correlated with pig fat accumulation, and positively correlated with the concentration of obesity-related metabolites in the serum. The bacterial colonization experiment in sterile mice proves that the bacteria is The causality of host fat accumulation. (@Szx)
[Original information]
Prevotella copri increases fat accumulation in pigs fed with formula diets
2021-08-21, doi: 10.1186/s40168-021-01110-0
Gut: transplant The gastric flora of patients with gastric cancer causes gastric cancer lesions in germ-free mice
Gut——[23.059]
The gastric juice samples were analyzed by sequencing the flora, and the results showed that the structure of the flora in different locations was similar; ② The flora was isolated from chronic superficial gastritis, intestinal metaplasia (IM), gastric tissue and gastric juice samples of GC and transplanted to no Bacteria in mice, the flora can be selectively colonized in the stomach of mice, transplantation of IM and GC flora can induce precancerous lesions; ③Characteristic changes include: significant reduction of parietal cells, aggregation of inflammatory cells, expansion of epithelial proliferation area and tissue Metaplasia, and obvious dysplasia after 1 year of colonization of the flora.
[Editor-in-Chief comment]
Gastric cancer (GC) is the leading cause of cancer-related deaths.Although bacteria other than Helicobacter pylori may also be involved in the occurrence of gastric cancer, wild-type sterile (GF) mouse models are used to study the role of human gastric flora in the occurrence of gastric cancer. The current research has not yet involved. Gut recently published an article that transplanting gastric flora from patients with intestinal metaplasia or GC into GF mice can reproduce the main histopathological features of precancerous lesions. The study suggests that the gastric flora can participate in the occurrence and development of gastric cancer, and GF mice can be used to study the causal relationship between the gastric flora and gastric diseases. (@爱的择择)
[Original information]
Human gastric microbiota transplantation recapitulates premalignant lesions in germ-free mice
2021-08-13, doi: 10.1136/gutjnl-2021-324489 hr
hr hr hr : New mechanism of enterotoxigenic Bacteroides fragilis to promote enteritis/cancer
hr : New mechanism of enterotoxigenic Bacteroides fragilis to promote enteritis/cancer
Gastroenterology——[22.682]
① Enterotoxigenic Bacteroides fragilis (ETBF) promotes colorectal cancer (CRC) cells by down-regulating miR-149-3p Proliferation and down-regulation of miR-149-3p by ETBF depends on the methylation of m6A mediated by METTL14; ② After ETBF stimulates CRC cells, the target gene of miR-149-3p, PHF5A, transactivates SOD2 by regulating the variable splicing of KAT2A mRNA ③ miR-149-3p can be released from exosomes and mediate intercellular communication by regulating Th17 differentiation; ④ From healthy controls to patients with inflammatory bowel disease (IBD) and CRC, the effect of miR-149-3p in plasma The level gradually decreased; ⑤ In patients with IBD and CRC, the miR-149-3p of plasma exosomes was negatively correlated with the abundance of ETBF.
[Editor-in-Chief comment]
Enterotoxigenic Bacteroides fragilis (ETBF) is closely related to the occurrence of inflammatory bowel disease (IBD), colitis-related colorectal cancer (CAC) and colorectal cancer (CRC).However, the mechanism by which ETBF induces intestinal inflammation and tumorigenesis remains unclear. Hong Jie and Chen Haoyan from Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and their team published a study on Gastroenterology and found that ETBF-stimulated cells deliver miR-149-3p through exosomes to promote Th17 cell differentiation. At the same time, ETBF promotes PHF5A-mediated variable cleavage of KAT2A by down-regulating miR-149-3p, thereby inducing colorectal cancer. These findings suggest that in patients with IBD and CRC infected with ETBF, the ETBF/miR-149-3p pathway may be a potential therapeutic target. (@爱的择择)
[Original information]
Enterotoxigenic Bacteroides fragilis promotes intestinal inflammation and malignancy by inhibiting exosomes-packaged miR-149-3p
2021-08-06, doi: 10.1053/j.gastro. 2021.08.003
Cell Sub-Journal: Why does the oral vaccine fail in environmental bowel disease?
Immunity——[31.745]
① Through low-protein-low-fat diet+adhesive invasive Escherichia coli treatment, the environmental intestinal dysfunction (EED) model was constructed, and the mice had growth retardation, enteritis, and oral vaccine failure; ② EED The oral vaccine response of CD4+ T cells in the small intestine but not in the lymph nodes is impaired, suggesting that the relevant inhibition is directed at the intestinal resident T and B cells; ③ The small intestine resident RORγT+Treg cell proliferation, accumulation, and intestinal flora disorders are all EED The prerequisite for the failure of oral vaccine; ④ The targeted deletion of RORγT+Treg can restore vaccine-specific CD4+T cell response and vaccine protection; ⑤ The deletion of RORγT+FOXP3+Treg can aggravate growth retardation, suggesting that RORγT is a key pathological factor.
[Editor-in-chief's comment]
Environmental intestinal dysfunction (EED) is a common intestinal inflammatory disease in poor children in developing countries, which can cause developmental delay. A recent article published by Immunity constructed an EED mouse model to study the pathology of related oral vaccine failures, and revealed the microbiota and diet-dependent immune regulation mechanisms. It is worth mentioning that, led by Jeffrey Gordon, taking this article as an example, more and more researches on the gut microbiome are now tilting towards research on intestinal health in developing countries and poor areas, such as child malnutrition. (@好雨)
【Original information】
Environmental enteric dysfunction induces regulatory T cells that inhibit local CD4+ T cell responses and impair oral vaccine efficacy
2021-08-03, doi: 10.1016/j.immuni. 2021.07.005
Nature Sub-Journal: Young intestinal flora may rejuvenate the aging brain
Nature Aging——[N/A]
① Intestinal flora, immunity, hippocampus nerve Occurrence/metabolome/transcriptome and behavior change with aging. Transplantation of fecal microbiota (yFMT) of young mice can partially improve these changes; ② yFMT changes the composition of the flora and specific intestinal-brain axis modules and the metabolic functions of the flora (such as SCFA) Metabolism); ③ yFMT partially restores peripheral immunity (especially mesenteric lymph node immune cells) and improves hippocampal microglial cell defects; ④ yFMT reverses the hippocampal metabolome (such as vitamin A, GABA, Neu5Gc, arginine and other metabolites) And related pathways) and changes in the expression of glutamine synthetase; ⑤ yFMT improves aging-related memory, learning and behavior defects.
[Editor's comment]
Intestinal flora is closely related to brain health and aging. Nature Aging recently published research work from John Cryan's team, focusing on comparing the flora, immunity (peripheral immunity + neuroimmunity), brain metabolome and gene expression, and behavior of fecal bacteria transplanted from young or old mice to old mice. The influence of the intestinal flora indicates that the young intestinal flora can partially reverse the brain function and behavior defects caused by aging through mechanisms such as metabolism and immunity, or it can bring new ideas for the intervention and treatment of related diseases. (@Mildbreeze)
[Original information]
Microbiota from young mice counteracts selective age-associated behavioral deficits
2021-08-09, doi: 10.1038/s43587-021-00093-9
Domestic team Intestinal flora characteristics of gout patients
NPJ Biofilms and Microbiomes——[7.29]
① Compared with healthy controls, the abundance of Prevotella, Fusobacterium and Bacteroides in the feces of gout patients increased , While the abundance of Enterobacteriaceae and butyric acid-producing bacteria decreased; ② the abundance of fructose and mannose metabolism and lipid A synthesis genes in gout patients increased, and the abundance of uric acid degradation and short-chain fatty acid synthesis genes decreased; ③ Enterobacteriaceae Reduce or reduce amino acid metabolism and environmental perception, and aggravate disease symptoms; ④ Random forest model based on three bacterial genes can predict gout more accurately; ⑤ Uric acid and anti-inflammatory drugs can partially restore the intestinal flora of patients; ⑥ and Compared with metabolic diseases, the gut flora of patients with gout is closer to those with autoimmune diseases.
[Editor-in-chief comment]
There is evidence thatThere is an association between gut flora and arthritis diseases (including gout). However, in gout, how and which bacteria in the gut affect host urate degradation and gout inflammation remain unclear. Wang Zhang from South China Normal University and Huang Qingchun and Huang Runyue from Guangdong Provincial Hospital of Traditional Chinese Medicine and their team published a study on NPJ Biofilms and Microbiomes. 307 fecal samples from 102 gout patients and 86 healthy controls were analyzed. Genomic analysis revealed that the gut microbiota structure of gout patients was significantly different from that of healthy controls, and was closer to other autoimmune disease patients, indicating that the imbalance of intestinal microflora is related to the imbalance of host urate degradation and systemic inflammation, or may be As a non-invasive diagnostic marker for gout. (@EADGBE)
[Original information]
Metagenomic analysis revealed the potential role of gut microbiome in gout
2021-08-09, doi: 10.1038/s41522-021-00235-2
more intake Lignan may reduce the risk of coronary heart disease
Journal of the American College of Cardiology——[24.094]
① Include 214,108 subjects in 3 cohorts, and undergo dietary assessment every 2-4 years; ② In During the follow-up period of 5,517,225 person-years, 10,244 cases of coronary heart disease occurred, including 6,823 cases of non-fatal myocardial infarction and 3,961 cases of fatal coronary heart disease; ③Total lignans, podocarlinin, saccharin, and rosinol The intake of larch resin alcohol was significantly negatively correlated with the risk of coronary heart disease. Compared with the lowest intake, the risk of coronary heart disease of the highest intake was significantly reduced by 15%, 24%, 13%, 11% and 11%; ④ In subjects with higher total fiber intake, the negative correlation between total lignan intake and coronary heart disease was more obvious.
[Editor-in-chief comment]
Lignans are mainly derived from the intake of plant-based diets.Especially seeds, whole grains, fruits, vegetables, tea, coffee, etc. According to the results of a prospective cohort study published in the Journal of the American College of Cardiology, more than 210,000 subjects were followed up for many years and found that lignan intake was significantly negatively correlated with the risk of coronary heart disease. (@Szx)
[Original Information]
Lignan Intake and Risk of Coronary Heart Disease
2021-08-09, doi: 10.1016/j.jacc.2021.05.049
Nature Sub-Journal: Induction 860 A study revealing the dietary risks of 11 primary cancers (review)
Nature Communications——[14.919]
① This umbrella review included 860 observational Meta-analysis to assess dietary factors and primary cancers at 11 anatomical sites The evidence strength of the association; ② Only a few single foods/nutrients and cancer are supported by strong or highly suggestive Meta-analysis evidence, and similar studies in the future are unlikely to change this evidence; ③ Strong or highly suggestive The evidence supports that drinking is positively related to the risk of colon cancer, rectal cancer, breast cancer, esophageal cancer, head and neck cancer, and liver cancer; ④ The intake of calcium, dairy products and whole grains is negatively related to the risk of colorectal cancer. Coffee is negatively associated with the risk of liver cancer and skin basal cell carcinoma.
[Editor-in-chief's comment]
More and more studies have shown that diet and nutrition are modifiable risk factors for a variety of cancers. An umbrella review recently published in Nature Communications assessed the evidence for the association between diet/nutrition and 11 primary cancers. (@陈彬林)
[Original information]
An umbrella review of the evidence associating diet and cancer risk at 11 anatomical sites
2021-07-28, doi: 10.1038/s41467-021-24861-8
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08-24 | Fighting "colitis": 8 articles at a glance recent important research progress
08-22 | Nutrition Review 9 Burst: The Science of Eating, Feeling Comprehend
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