Gut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease

Gut Microbes. 2021 Jan-Dec;13(1):1990827. doi: 10.1080/19490976.2021.1990827.

Abstract

Intestinal epithelium represents a dynamic and diverse cellular system that continuously interacts with gut commensals and external cues. Intestinal stem cells, which lie at the heart of epithelial renewal and turnover, proliferate to maintain a steady stem cell population and differentiate to form functional epithelial cell types. This rather sophisticated assembly-line is maintained by an elaborate micro-environment, sculpted by a myriad of host and gut microbiota-derived signals, forming an intestinal stem cell niche. This complex, yet crucial signaling niche undergoes dynamic changes during homeostasis and chronic intestinal inflammation. Inflammatory bowel disease refers to a chronic inflammatory response toward pathogenic or commensal microbiota, in a genetically susceptible host. Compositional and functional alterations in gut microbiota are pathognomonic of IBD.The present review highlights the modulatory role of gut microbiota on the intestinal stem cell niche during homeostasis and inflammatory bowel disease. We discuss the mechanisms of direct action of gut commensals (through microbiota-derived or microbiota-influenced metabolites) on ISCs, followed by their effects via other epithelial and immune cell types.

Keywords: Intestinal epithelial stem cells (ISCs); crypt specific core microbiota CSCM); enteroendocrine cells; gut metabolites; gut microbiota; inflammatory bowel disease (IBD); mesenchyme; paneth cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Gastrointestinal Microbiome*
  • Humans
  • Inflammatory Bowel Diseases / metabolism
  • Inflammatory Bowel Diseases / microbiology*
  • Inflammatory Bowel Diseases / physiopathology
  • Intestinal Mucosa / cytology*
  • Intestinal Mucosa / microbiology
  • Stem Cell Niche*
  • Stem Cells / cytology
  • Stem Cells / metabolism

Grants and funding

This work was supported by the Science and Engineering Research Board (SERB), Department of Science and Technology, under Grant CRG/2019/005292; and Scheme for Promotion of Academic and Research Collaboration (SPARC), Ministry of Human Resource Development, under Grant 1498.