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Atlas of the aging mouse colon

ABSTRACT: Colon cancer is one of the leading causes of death within the western world and is linked to the aging of the colon. The disease presents differently between men and women, developing in different parts of the colon and often with a different morphology. The colonic epithelium is a rapidly renewing tissue, tasked with absorption of water and nutrients, interacting with a wide array of intestinal microbes. The gut-associated lymphoid tissue houses the majority of all immune cells. These immune cells interact with and help regulate the activity of epithelial cells. However, not much is known whether compartment-specific changes occur during aging and how said changes could impact the epithelium. Here we show that both epithelial and immune cells differ significantly between colonic compartments and experience age-related changes, with the possible causal interactions. We found a shift in the absorptive-secretory cell balance, the decrease in colonocytes possibly linked to age-associated malabsorption and intestinal disturbances. We demonstrate marked changes in the aging of the immune cells with regard to populations and interactions with epithelial cells, linking aged immune cell produced cytokines (Ifn-γ, Il1B) and the aging of colonic epithelium, which lines up with observations of inflammation causing or exacerbating age-associated gut disfunctions, such as colon cancer. Our results provide new insights into the normal and age-associated states of the colon. We anticipate our work will provide a foundation for further inquiry not only into diseases of the colon (even outside the realm of aging research) but developmental research as well.

ORGANISM(S): Mus musculus

PROVIDER: GSE168448 | GEO | 2022/03/31

REPOSITORIES: GEO

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Project description:The mammalian gut harbors a diverse microbial community (gut microbiota) that mainly consists of bacteria. Their combined genomes (the microbiome) provide biochemical and metabolic functions that complement host physiology. Maintaining symbiosis seems to be a key requirement for health as dysbiosis is associated with the development of common diseases. Previous studies indicated that the microbiota and the hostM-bM-^@M-^Ys epithelium signal bidirectional inducing transcriptional responses to fine-tune and maintain symbiosis. However, little is known about the hostM-bM-^@M-^Ys responses to the microbiota along the length of the gut as earlier studies of gut microbial ecology mostly used either colonic or fecal samples. This is of importance as not only function and architecture of the gut varies along its length but also microbial distribution and diversity. Few recent studies have begun to investigate microbiota-induced host responses along the length of the gut. However, these reports used whole tissue samples and therefore do not allow drawing conclusions about specificity of the observed responses. Which cells in the intestinal tissue are responsible for the microbially induced response: epithelial, mesenchymal or immune cells? Where are the responding cells located? We used using extensive microarray analysis of laser capture microdissection (LCM) harvested ileal and colonic tip and crypt fractions from germ-free and conventionally-raised mice to investigate the microbiota-induced transcriptional responses in specific and well-defined cell populations of the hostM-bM-^@M-^Ys epithelium. Ileum and colon segments were dissected from germ-free and conventionally-raised 10-12 weeks old female C57Bl/6 mice, washed and frozen as OCT blocks. Cryosections were prepared from these OCT blocks and tip/crypt fractions isolated using laser capture microdissection. To investigate the microbiota-induced transcriptional responses specific for specific subpopulations of intestinal epithelial cells, tip and crypt fractions of ileal and colonic epithelium of germ-free and conventionally-raised 10-12 weeks old female C57Bl/6 mice were harvested using laser capture microdissection and probed in an extensive microarray analysis.

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Atlas of the aging mouse colon

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