A gut bacterium protects aging lungs from scarring

Pulmonary fibrosis develops when repeated lung tissue injury activates cells that overproduce connective tissue. Collagen plays a central role: the structural protein that normally provides support instead accumulates in the small air sacs of the lung. The researchers, whose findings appeared in the journal Aging Cell, used a bacterial strain called L9, originally isolated from centenarians. They administered this bacterium to mice between 15 and 24 months of age.

Collagen dropped by 40 percent

Without intervention, 24-month-old mice developed intense pulmonary fibrosis. In mice given L9, the total fibrosis score was only 70% of that seen in the control group. The amount of collagen fibres decreased by 40%. This effect worked through a reduction in PINP, a collagen precursor, and a decline in LOX, an enzyme that cross-links collagen fibres.

The bacterium drove these changes via the gut-lung axis: a route by which metabolic products of gut bacteria enter the bloodstream and influence organs elsewhere in the body. This is the same route through which gut bacteria also communicate with the brain and immune system.

Aging makes lungs more vulnerable

The study also showed that older people already had more collagen deposition in their lungs, even when these were considered normal samples. Genes involved in producing components of the extracellular matrix (the support tissue between cells) were more active in older lung samples. This suggests that aging itself makes lung tissue more susceptible to fibrosis, before disease even begins.

These findings are preliminary and apply only to mice so far. Whether L9 produces comparable effects in humans has not yet been studied. From a longevity perspective, it is noteworthy that a gut microbe appears able to limit age-related damage in another organ via an indirect route, though the researchers themselves are cautious about broader implications.

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