Gut Microbes Contribute to Age-Associated Inflammation
Inflammation increases with age and is a strong risk factor for death in the elderly, but the underlying cause has not been clear. A study published April 12th, 2017 in Cell Host & Microbe reveals that gut microbes are one of the culprits behind age-associated inflammation and premature death in mice. Imbalances in the composition of gut microbes in older mice cause the intestines to become leaky, allowing the release of bacterial products that trigger inflammation and impair immune function.
A release from the publisher quotes senior author Dawn Bowdish of the Michael G. DeGroote Institute for Infectious Disease Research at McMaster University in Canada as saying, “To date, the only things you can do to reduce your age-associated inflammation are eat a healthy diet, exercise, and manage any chronic inflammatory conditions to the best of your ability. We hope that in the future we will be able use drugs or pre- or probiotics to increase the barrier function of the gut to keep the microbes in their place and reduce age-associated inflammation and all the bad things that come with it.”
The release notes that age is associated with an increase in levels of tumor necrosis factor (TNF) and other pro-inflammatory cytokines in the bloodstream and tissues. Individuals with high levels of these inflammatory molecules are more likely to be frail, hospitalized, and less independent; are more susceptible to certain types of infections; and have a variety of chronic, late-life diseases such as dementia and cardiovascular disease, as well as higher death rates. Some have proposed that age-associated inflammation is caused by accumulating wear and tear on our immune cells, while others have suggested that it is caused by immune cells dealing with chronic viral infections. But evidence supporting these hypotheses has been elusive, and the underlying cause of age-associated inflammation has remained unknown.
Bowdish and her colleagues raised mice in germ-free conditions and compared them to their conventionally raised counterparts. Strikingly, the germ-free mice did not show an age-related increase in intestinal permeability or in levels of bacterial products or pro-inflammatory cytokines in the bloodstream, in contrast to conventionally raised mice. Moreover, a higher proportion of germ-free mice lived to the ripe old age of 600 days, and macrophages derived from older germ-free mice maintained anti-microbial activity. Taken together, these findings demonstrate that age-related changes in the gut microbiome weaken the intestinal barrier, leading to the release of bacterial products that promote inflammation, impair immune function, and reduce lifespan.