New study suggests why elderly adults are more susceptible to flu

With ageing, an inflammatory lipid appears to diminish the amount of macrophages inside the lungs.
The study, led by first author Judy Chen, a Ph.D. candidate, senior author Daniel Goldstein, M.D., the Eliza Maria Mosher Collegiate Professor in Internal Medicine and Professor of Microbiology and Immunology, and their team, looks into why cells known as alveolar macrophages, the lungs’ first line of defence, appear to be compromised with age.

These macrophages are immune cells that dwell in the tiny air sacs, or alveoli, inside the lungs and assault invaders like the flu virus. Importantly, these cells appear to be lost as people age. Another study found that when macrophages from an aged mouse were transplanted into a young mouse, the cells appeared young again. “This led us to conclude that something in the lungs’ environment was contributing to this,” Chen explained. Prostaglandin E2 (PGE2), a lipid immune modulator with wide-ranging effects ranging from labour induction in pregnancy to arthritic inflammation, was implicated. The researchers observed that PGE2 levels in the lungs increase with ageing.

This rise in PGE2, according to Chen, affects lung macrophages, decreasing their general health and capacity to produce.
The researchers believe that the accumulation of PGE2 is yet another indication of senescence, a biological condition that occurs with age. Senescence protects against the uncontrolled division of damaged cells; senescent cells can no longer reproduce. “One of the fascinating aspects of these cells is that they release a lot of inflammatory substances,” Chen explained.

The study found that as people age, the cells lining the air sacs in their lungs become senescent, resulting in increased PGE2 production and immunological suppression. They injected aged mice with a medication that disables a PGE2 receptor to evaluate the relationship between PGE2 and greater susceptibility to influenza. “The aged mice that had that treatment had more alveolar macrophages and survived influenza infection better than the older animals that didn’t get the therapy,” Chen explained.

The researchers will now look at how PGE2 impacts lung macrophages and its possible function in inflammation throughout the body. “As we age, we become more vulnerable not only to influenza, but also to other infections, malignancies, and autoimmune illnesses.”