Short-chain fatty acids play a beneficial role in the gut-lung axis of aging mice

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The gut microbial community structure-; communities of bacteria, viruses and fungi that live in the intestines-; influences the inflammatory response in the lungs of aging mice, according to researchers from the Institute of Functional Anatomy at Charité, the Medical University of Berlin in Germany. The study is published in the American Journal of Physiology-Lung Cellular and Molecular Physiology and has been chosen as an APSselect article for May.

The findings emphasize the importance of the intestinal microbiome and its metabolic function in healthy aging."

Christina Brandenberger, PhD

Inflammation leads to reduced lung function and disease in older adults. It also worsens their prognosis in cases of pneumonia and acute lung injury. However, the source of the inflammation and potential treatments are not fully understood.

In this study, researchers analyzed the gut microbiome and its impact on inflammatory signaling in aging lungs. Then, scientists tested the effects of short-chain fatty acids (SCFAs)-;beneficial metabolites of the gut microbiome-;in mice ages three to 18 months. The animals drank either water mixed with SCFAs or water only. The researchers discovered that inflamm-aging (chronic, low-grade inflammation that develops during aging) in the lungs of healthy, old mice was reduced when they were supplemented with SCFAs. The research team also found an improvement in pulmonary inflammation severity in older mice with acute lung injury.

"This study provides new evidence that SCFAs play a beneficial role in the gut-lung axis of the aging organism by reducing pulmonary inflamm-aging and ameliorating enhanced severity of acute lung injury in older mice," this study's authors wrote. Researchers said these findings could help improve human health as it relates to pulmonary aging by focusing on gut bacteria.

Journal reference:

Fagiola, M., et al. (2023) The relationship between elastin cross linking and alveolar wall rupture in human pulmonary emphysema. American Journal of Physiology-Lung Cellular and Molecular Physiology.


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