11 November 2022

Aging immunity

Scientists have found out why old people catch colds more often

Sergey Vasiliev, Naked Science

Winter is approaching, and with it — another increase in the number of patients with flu and other colds. They are especially dangerous for the elderly, who are more likely to become infected and tolerate the disease worse. Scientists from the University of Michigan managed to link this to the reduced activity of alveolar macrophages, which play the role of the first line of defense of our lungs. The article by Daniel Goldstein and his colleagues was published in the journal Nature Communications (Chen et al., Age-induced prostaglandin E2 impairs mitochondrial fitness and increases mortality to influenza infection).

Macrophages are immune cells capable of moving independently, actively capturing and absorbing various pathogens. They are present in almost all organs and tissues, "specializing" in protecting their part of the body. Especially important tasks have to be solved by alveolar macrophages, which inhabit the lungs and "clean" them from everything that gets inside with air, including influenza viruses.

In people over 65 years of age, the activity of alveolar macrophages noticeably decreases, which leads to a weakening of their protection against influenza and colds in general. At the same time, experiments show that if the macrophages of old mice are transplanted into young ones, they become active again. Obviously, some factors present in the environment of the lungs determine the state of immune cells.

One of the regulators of their activity is prostaglandin E2 (PGE2). Goldstein and his co-authors have shown that with age, the amount of this mediator in the lungs increases, reducing the activity of macrophages and their ability to multiply. Scientists associate this with the development of senescence processes — cellular aging.

With age, damage accumulates in the DNA, and in order to reduce the risks associated with this, the cells switch to the "senescent mode". Division stops, the synthesis of substances associated with inflammatory reactions and oxidative stress is activated. In old age, more and more cells become senescent, which leads to profound changes in the whole body. The authors of the new work demonstrated that senescent lung cells produce PGE2 more actively, and this, in turn, leads to suppression of macrophage activity.

This was proved in experiments on mice that were blocked by PGE2 receptors. In elderly rodents treated with such a drug, the number of macrophages remained quite high, and they more often survived after infection with influenza than peers in whom PGE2 acted as usual. Perhaps in the future, medications that weaken the effect of PGE2 will help protect the elderly as well.

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