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Why do older people get sicker with the flu or Covid?

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Researchers of the University of California, in San Francisco, have studied the mechanisms by which older people become more seriously ill when infected with respiratory pathogens.

In his study, published in the journal Immunityhave tried to unravel the structural bases of what is known as inflammation –chronic inflammation associated with aging–.

Research shows that, as the years go by, the activation of a specific element – ​​nuclear factor NF-κB – in fibroblasts – essential cells for maintaining the integrity of skin and organs – completely remodels the architecture of the immune system.

This process would act as a domino effect: the alteration triggers the appearance of new lymphoid structures in the lung and promotes a population of “exhausted” immune cells –CD8+ GZMK+ T cells–.

This cell population is different from that which arises during a chronic viral infection, but is closely linked to both normal aging and to cases of cancer and autoimmunity.

Melatonin could reduce mortality in critically ill patients with COVID-19. Photo: Europa Press.

And at a clinical level, this aging of the immune system drastically increases the body’s susceptibility to suffer acute lung injuries.

In fact, this cellular mechanism imitates and explains the symptoms of severe pneumonia. This discovery opens an important therapeutic avenue for the future.

Researchers have found that by depleting or eliminating these aging T cells, lung vulnerability is relieved.

The finding places fibroblasts as the true “orchestral conductors” of immunological aging in non-immune tissues, providing the key to understanding – and potentially treating – our vulnerability to age-related diseases.

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