in humans. In contrast, young germ-free mice that received gut microbes from other young mice did not experience the same increase in inflammation.The research indicates that alterations in the gut microbiome may contribute to the widespread inflammation that commonly accompanies aging. The study, published in the journal Aging Cell, also revealed that antibiotics had a more enduring impact on the gut microbiomes of older mice compared to younger mice. Jacob Allen, a professor of kinesiology and communication, noted that there is a growing agreement that aging is linked to a gradual rise in chronic low-grade inflammation. This was observed in germ-free mice that were transplanted with microbes from other mice of the same age, and no increase in inflammation was recorded.The new research was led by Dr. Jeffrey Woods, a professor of kinesiology and community health at the University of Illinois Urbana-Champaign, and Thomas Buford, a professor of medicine at the University of Alabama at Birmingham. They sought to understand the underlying cause of the aging-induced inflammatory state and its relationship to the functional capacity of the microbiome. Previous studies have already linked age-related changes in gut microbial composition to chronic inflammatory diseases like Parkinson’s and Alzheimer’s.illness. There have been some research that have connected the way microorganisms break down substances in the body to a person’s susceptibility to other health issues, such as obesity, irritable bowel syndrome, and heart disease. The changes in the gut microbiome that happen as a person ages may also play a role in causing the so-called leaky gut problem, the scientists explained.
“The patterns of microorganisms in older mice are strongly linked to indications of bacteria-caused barrier disruption and immune infiltration,” they stated.
“The substances that exist in our gut are meant to be kept separate from the rest of our body,” Buford mentioned. “If they escape, our immune system will identify them. ”
Many research studies have compared the variety and quantity of different types of microorganisms in the gut. This provides important information about the groups that can affect health or disease. However, analyzing the microbes in the gut can be expensive and the results can be hard to understand. This is why Allen and his team decided to study the function of the microbes, specifically how the gut microbiomes of aging mice might trigger an immune response.
The focus of the team was on toll-like receptors, which are molecules that play a role in inflammatory processes.within the body. TLRs are located in the membranes of cells and are responsible for examining the external environment for indications of tissue damage or infection. When a TLR comes into contact with a molecule linked to a potential pathogen, such as the lipopolysaccharide component of a gram-negative bacterium, it triggers an innate immune response by recruiting pro-inflammatory agents and other molecules to combat the infection.
The scientists initially investigated whether the contents of the colon in young and old mice were inclined to stimulate TLR signaling. They discovered that the microorganisms in older mice were more likely to activate TLR4, which detects lipopolysaccharides.The researchers discovered that the lipopolysaccharide components of bacterial cell walls were affected differently in aged and young mice. However, a different receptor called TLR5, which senses flagellin, was not affected differently based on age. When young germ-free mice were given the microbes of aged mice, they also had higher inflammatory signaling and increased levels of lipopolysaccharides in their blood. This supports the idea that aging-induced changes in microbiota can lead to increased inflammation in the host. In additional experiments, the researchers treated mice with broad-spectrum antibiotics and tracked changes in their microbiota.The research found significant changes in the microbiomes during treatment and for seven days afterward.
Buford expressed his interest in what microbes return immediately after the antibiotic treatment ends. In mice with aged microbiota in their guts, the opportunistic pathogens were the quickest to return.
Allan noted the importance of the findings, stating that as we age, our microbiome may be less resilient to antibiotic challenges, especially considering the increased exposure to antibiotics in Western societies.The researchers stated that understanding the impact of age-related microbial changes in the gut on long-term health and inflammation is an important step. The study’s coauthors included Elisa Caetano-Silva, a postdoctoral researcher at Illinois; Akriti Shrestha, a Ph.D. student at the U. of I.; Michael Bailey, a research scientist at the National Children’s Hospital; and Jeffrey Woods, the director of the Center on Health, Aging and Disability at Illinois. Allen, who is also a professor of nutritional sciences at Illinois, and an affiliate of the Carl R. Woese Institute for Genomic Biology at the U. of I., was also involved in the study. The research was supported by the National Institutes of Health.
