To What Degree do Bodily Microbiomes Beyond the Gut Contribute to the Chronic Inflammation of Aging?

Most research on the microbial life of the body in the context of aging is focused on the gut microbiome, though a fair amount of investigation of oral microbial populations also takes place. In both cases, changes occur with age that allow harmful species of microbe to prosper, contributing to the chronic inflammation of aging. In the case of the gut microbiome, fecal microbiota transplantation from young individuals to old individuals has been shown in animal studies to reverse detrimental changes and improve health and life span. This has yet to be earnestly attempted for other microbial populations of the body that plausible contribute meaningfully to health, but the attempt should be made.

The human body and its microbiome represent an integrated meta-organism, which results from million years of reciprocal adaptation and functional integration conferring significant advantages for both parties. All the members of this human microbiota participate in host physiology and change according to development and late in the life contributing to health and fitness. The human immune system is influenced by the microbiota assembly, composition, diversity, and dynamics, and the interaction of all these features plausibly contributes to the process of inflammaging. In the last decades, we experienced an explosion of studies on the role of the gut microbiome in health and disease and the relationship between the gut microbiome and the other organs and tissues also due to an improvement of the sequencing methods that can be applied to the study of microbiota.

The complex relationship between humans and the trillions of bacterial cells that form our microbiome remains largely unexplored. The consequences for medicine are challenging, since it is likely that our multifaceted symbiosis affects each aspect of health. Manipulating the intestinal microbiota and microbiome may be helpful for preserving health and treating disease, particularly among older adults. On the contrary, the relationship between the microbiome of other human ecological niches (i.e., oral cavity, lung, skin, vagina, and genito-urinary tract) and the progress of other clinical diseases that are common among older adults remains an important area of future studies. It is also necessary to consider how biological age (assessed by health status and life expectancy) shapes the microbiota and immune system and vice versa. Moreover, the complexity of the interactions within the microbiome of the different body sites and between microbes and hosts presents a major challenge; a more concerted and predictive theoretical framework is imperative to progress.

Efforts to standardize specimen preparation and analytical protocols and to increase the availability of the growing body of data should be increased. These technical efforts as well as robust clinical research will improve characterization of the variation in the global human microbiomes, functions of redundancy, disease biomarkers, immigration, effect of lifestyles, and trajectories of development, all of which will establish the basis to understand the progression from health to disease and to efficiently discover new preventive strategies and therapies.

Link: https://doi.org/10.1007/s00281-020-00814-z

Comments

The majority of aging is likely caused by the microbiome, the rest is environmental and lifestyle. There is no such thing as a sterile animal or anything else for that matter. Microbial DNA is found in many more sites than listed in the paper; joints, blood, brain, organs, arterial plaque etc.

"Based on Tetz's theory of longevity, we propose that lifespan and aging are defined by the accumulation of alterations over all genes of macroorganism and microbiome and the non-living genetic elements associated with them."

" lifespan is the time required for the accumulation of alterations in the Individual Pangenome to the limiting value that is not compatible with life"

https://link.springer.com/article/10.1007/s12064-018-0267-4

Posted by: Lee at October 12th, 2020 8:34 AM

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