(ORDO NEWS) — Although the COVID-19 pandemic has provided a brief respite, the influenza virus is once again a major seasonal threat and, as usual, poses a risk to people over 65 years of age. But why are older people more susceptible to it?
A study led by professors and doctors of medical sciences from the University of Michigan (Judy Chen, Daniel Goldstein, Eliza Marie Mosher), USA, shows why special cells – alveolar macrophages – which form the first line of defense in the lungs, are severely damaged with age.
These macrophages are immune cells that attack external “invaders” such as influenza virus and live in small air sacs/alveoli inside the lungs. It is noted that these cells are “wasted” with age.
Previous studies have shown that when macrophages from an old mouse are placed in a young mouse, the cells seem to rejuvenate. “It led us to believe that something in the lung environment is contributing to this,” says Judy Chen.
Signs pointed to a lipid immunomodulator known as prostaglandin E2 (PGE2), with a wide range of effects, from induction of labor during pregnancy to inflammation in arthritis.
The research team found that the amount of PGE2 in the lungs increases with age. And this very increase in PGE2, as Chen explains, acts on macrophages in the lungs, limiting their overall health and ability to generate new cells.
The team suspects that the accumulation of PGE2 is another marker of a biological process that is often observed with age – that is, a marker of aging, which, in turn, serves as insurance against the uncontrolled division of damaged cells.
That is, senescent cells are no longer capable of replication and are less of a threat to the body.
Health in old age
“One of the interesting things about these cells is that they trigger a lot of inflammatory factors,” said Judy Chen.
So, the study showed that with age, the cells surrounding the air sacs in the lungs become senescent, and these same cells lead to an increase in the production of PGE2 and suppression of the immune response.
To test the link between PGE2 and increased susceptibility to influenza, the scientists treated aged mice with a drug that blocks the PGE2 receptor.
“Older mice treated with this drug actually had more alveolar macrophages and were better at surviving influenza infection than older mice not treated with the drug,” they said.
Going forward, the team plans to investigate the different ways PGE2 affects lung macrophages, as well as its potential role in inflammation throughout the body.
“With age, we become more susceptible not only to influenza, but also to other infections, cancer, autoimmune diseases, [therefore, it is important to study the effect of PGE2],” the scientists concluded .
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