Regulation of goblet cells by diet and microbiota derived metabolites
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Date
2025-05
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The Ohio State University
Abstract
Trillions of commensal microbes, collectively called microbiota, reside in the mammalian intestine. Microbiota break down dietary components to produce metabolites that regulate the symbiotic relationship between the host and microbiota. Intestinal epithelial cells (IECs) reside at the direct interface between the host and microbiota and respond to metabolites from the diet and microbiota. We hypothesize that diet and microbiota-derived metabolites regulate goblet cells within the Intestine.
We found mice fed rice bran exhibited decreased numbers of goblet cells, which are the specialized IEC that maintains mucosal barrier function through secretion of the compound mucin. Furthermore, rice bran feeding resulted in reduced epithelial expression of the gene Mucin 2 (Muc2).
Rice bran is known to contain high amounts of both fiber and phytate. Microbial fermentation of dietary fiber produces the short chain fatty acid (SCFA) butyrate. In addition, dietary phytate is digested by distinct microbial enzymes to produce phosphorous and inositol phosphate metabolites. Interestingly, utilizing in vitro culture systems employing a human colonic epithelial cell line, we found that butyrate inhibited goblet cell gene expression. On the other hand, phytate metabolites promoted the goblet cell gene Muc2 expression. When treated with both butyrate and phytate, the phytate effect was overridden by the butyrate effect. Thus, our results suggest that rice bran can decrease goblet cells in the colon through microbial metabolism of fiber, despite opposing effects by phytate
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Keywords
Immunology, Microbiota, Animal model, cell culture, Large intestine, epithelial cell