Scientists have found why old people catch colds more often

(ORDO NEWS) — Influenza and other colds are especially dangerous for older people due to the reduced activity of macrophages in their lungs.

Biologists have attributed this to the accumulation of senescent cells that secrete prostaglandin, which weakens the defense. If you use drugs that block it, then old mice suffer the flu almost the same as young ones.

Winter is coming, and with it another increase in the number of patients with influenza 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 have been able to attribute this to reduced activity of alveolar macrophages, which play the role of the first line of defense of our lungs.

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.

Particularly important tasks have to be solved by alveolar macrophages that inhabit the lungs and “cleanse” them from everything that gets inside with air, including influenza viruses.

In people over 65, the activity of alveolar macrophages drops markedly, 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 E 2 (PGE2). Goldstein and co-authors showed that with age, the amount of this mediator in the lungs increases, reducing the activity of macrophages and their ability to multiply.

Scientists attribute this to the development of senescence processes – cellular aging.

With age, DNA damage accumulates, and to reduce the associated risks, cells go into “senescent mode.”

The 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 throughout the body.

The authors of the new work demonstrated that senescent cells of the lungs produce PGE2 more actively, and this, in turn, leads to the suppression of macrophage activity.

This was proved in experiments on mice that were blocked with PGE2 receptors.

In elderly rodents treated with this drug, the number of macrophages remained quite high, and they more often survived after infection with influenza than their peers, in which PGE2 functioned normally.

Perhaps in the future, drugs that reduce the effects of PGE2 will help protect older people as well.


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