Editor's recommendation: Studies have found that inflammatory lipids appear to reduce the number of macrophages in the lungs as they age.
Although the COVID-19 pandemic provided a brief respite, the flu virus began to spread again and poses a particularly dangerous situation for people over the age of 65 as usual. But why are the elderly more likely to get influenza ? A new study published in the journal Nature Communications at the University of Michigan School of Medicine provides clues.
The study was led by first author Judy Chen PhD candidate, senior author Daniel Goldstein, MD, professor of internal medicine at Eliza Maria Mosher College and microbiology and professor of immunology, whose team investigated why alveolar macrophages, the first line of defense in the lungs, gets damaged with age.
These macrophages are immune cells that attack invaders such as influenza viruses, small air sacs that live in the lungs or alveoli . Importantly, these cells appear to disappear with age.
Previous research by another group showed that when macrophages from older mice were implanted into young mice, the cells looked younger again. "This prompted us to believe that something in the lung environment is what causes this condition," Dr. Chen noted. "
shows that a lipid immunomodulator called prostaglandin E2 (PGE2) has a wide range of effects, ranging from pregnancy induction to inflammation of arthritis. The team found that as we age, the amount of PGE2 in the lungs increases. Chen explained that the increase in PGE2 acts on macrophages in the lungs, limiting their overall health and production capacity. The
research team suspected that the accumulation of PGE2 is another sign of a biological process known as aging, which is often associated with age. Aging is an insurance to prevent damaged cell division from getting out of control; aging cells can no longer replicate.
"Interestingly, these cells secrete a large number of inflammatory factors".
study shows that as we age, cells in the air sacs in the lungs begin to age, which leads to an increase in PGE2 production and inhibits the immune response.
To test the link between PGE2 and increasing susceptibility to influenza, they treated elderly mice with a drug that blocks the PGE2 receptor. "Aging mice injected with this drug actually have more alveolar macrophages and have better survival rates in influenza infections than older mice without this drug," Chen said. The
research team plans to study the various ways PGE2 affects lung macrophages and its potential role in systemic inflammation. "As we get older, we are not only more likely to be infected with influenza, but also more likely to be infected with other infections, cancer and autoimmune diseases."
Source: Nature Communications
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