Washington [US]Nov 12 (ANI): An inflammatory lipid appears to reduce the number of macrophages inside the lungs with age.
The study, led by first author Judy Chen, Ph.D. candidate, lead author Daniel Goldstein, MD, associate professor of internal medicine Eliza Maria Mosher and professor of microbiology and immunology, and their team investigate why cells called alveolar macrophages, the first line of defense of the lungs, seem to be compromised with age. .
These macrophages are immune cells that attack invaders like the flu virus and live in the tiny air sacs, or alveoli, inside the lungs. Importantly, these cells appear to be lost with aging.
Previous research by another group showed that when macrophages from an old mouse were put into a young mouse and the cells looked young again. “This led us to believe that something in the lung environment is contributing to this,” Chen said.
Signs pointed to a lipid immune modulator known as prostaglandin E2 (PGE2) with wide-ranging effects, from induction of labor in pregnancy to inflammation with arthritis. The study team found that there is more PGE2 in the lungs with age. This increase in PGE2, Chen explained, acts on the lung’s macrophages, limiting their overall health and reproductive capacity.
The team suspects that the accumulation of PGE2 is another marker of a biological process called senescence, which is often seen with age. Senescence serves as insurance against the uncontrolled division of damaged cells; cells that are senescent can no longer replicate.
“One of the interesting things about these cells is that they secrete a lot of inflammatory factors,” Chen said.
The study showed that with age, the cells that line the air sacs of the lungs become senescent, and these cells lead to increased production of PGE2 and suppression of the immune response.
To test the link between PGE2 and increased susceptibility to the flu, they treated older mice with a drug that blocks a PGE2 receptor. “Old mice that received this drug ended up having more alveolar macrophages and had better survival from influenza infection than older mice that did not receive the drug,” Chen said.
The team next plans to investigate the different ways in which PGE2 affects lung macrophages, as well as its potential role in inflammation throughout the body. “As we age, we become more susceptible not only to the flu, but also to other infections, cancers and autoimmune diseases.” (ANI)
This report is automatically generated from the ANI news service. ThePrint is not responsible for its content.