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Bacterial Sphingolipids Exacerbate Colitis by Inhibiting ILC3-derived IL-22 Production.

Bin Bao1, Youyuan Wang2, Pavl Boudreau3

  • 1Division of Gastroenterology, Hepatology, and Nutrition; Boston Children's Hospital, and Harvard Medical School, Boston, Massachusetts; Division of Infectious Diseases, Boston Children's Hospital, and Harvard Medical School, Boston, Massachusetts; School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, Anhui, China.

Cellular and Molecular Gastroenterology and Hepatology
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PubMed
Summary
This summary is machine-generated.

Bacterial sphingolipids from Bacteroides fragilis worsen gut inflammation. Removing these sphingolipids in mice reduced colitis severity by boosting protective immune responses, highlighting their role in mucosal immunity.

Keywords:
ColitisIL22ILC3 CellsMicrobiotaSphingolipids

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Area of Science:

  • * Gastroenterology and Immunology
  • * Microbiome-Host Interactions

Background:

  • * Gut bacterial sphingolipids, produced by Bacteroidetes, have complex roles in virulence and host immunity.
  • * Altered sphingolipid profiles are observed in inflammatory bowel disease (IBD) patients.
  • * The precise mechanisms by which bacterial sphingolipids regulate intestinal homeostasis and inflammation are not fully understood.

Purpose of the Study:

  • * To investigate the role of Bacteroides fragilis sphingolipids in modulating intestinal inflammation.
  • * To elucidate the impact of bacterial sphingolipids on host mucosal immune responses.

Main Methods:

  • * Utilized a dextran sodium sulfate (DSS)-induced colitis mouse model, monocolonized with B. fragilis strains with or without sphingolipids.
  • * Employed transcriptional, protein, and cellular analyses, including colonic explants and organoids.
  • * Assessed host immune cell populations, cytokine profiles (e.g., IL-22, IL-18), epithelial STAT3 activity, and cell proliferation.

Main Results:

  • * Mice colonized with B. fragilis lacking sphingolipids showed significantly reduced DSS-induced colitis severity.
  • * Absence of sphingolipids correlated with increased interleukin-22 (IL-22) production by innate lymphoid cells (ILC3).
  • * B. fragilis sphingolipids were found to impede epithelial IL-18 production and suppress IL-22 release from specific ILC3 subsets.

Conclusions:

  • * B. fragilis-derived sphingolipids exacerbate mucosal inflammation.
  • * This exacerbation occurs through the inhibition of epithelial IL-18 expression.
  • * Bacterial sphingolipids also suppress IL-22 production by ILC3 cells, contributing to intestinal inflammation.