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RhoB affects colitis through modulating cell signaling and intestinal microbiome.

Jianming Yang1, Geng Pei1, Xuan Sun1

  • 1Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Immunology, Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, 22 Qixiangtai Road, Heping District 300070, Tianjin, 300070, China.

Microbiome
|September 16, 2022
PubMed
Summary

RhoB protein is elevated in ulcerative colitis (UC) and drives disease development. Reducing RhoB in colitis models improved gut healing and altered the microbiome, suggesting RhoB as a potential UC therapeutic target.

Keywords:
Inflammatory bowel diseasesMicrobiomeRhoBSCFAs

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Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Microbiome Research

Background:

  • Inflammatory bowel diseases (IBD), including ulcerative colitis (UC), have complex causes, and effective diagnostic and treatment options are still needed.
  • The function of RhoB, a regulator of cell processes, in the context of colitis remains largely unknown.

Purpose of the Study:

  • To investigate the role of RhoB in the pathogenesis of ulcerative colitis (UC).
  • To explore RhoB as a potential biomarker and therapeutic target for UC.

Main Methods:

  • Quantification of RhoB expression in colon tissues from UC patients and DSS-induced colitis mouse models.
  • Assessment of colitis severity, goblet cell numbers, and intestinal epithelial cell (IEC) proliferation in wild-type, RhoB+/- , and RhoB-/- mice.
  • Analysis of Wnt signaling and p38 MAPK signaling pathways.
  • Characterization of the gut microbiome composition and short-chain fatty acid (SCFA) concentrations.

Main Results:

  • RhoB levels were significantly increased in the colons of UC patients and DSS-induced colitis mice.
  • Mice with reduced RhoB (RhoB+/- and RhoB-/-) exhibited milder colitis, increased goblet cell numbers, and enhanced IEC proliferation.
  • Lower RhoB expression promoted goblet cell differentiation and epithelial repair by inhibiting the Wnt pathway and activating the p38 MAPK pathway.
  • Mice with reduced RhoB showed an increase in SCFA-producing bacteria and SCFA levels, alongside upregulated SCFA receptor expression.

Conclusions:

  • Elevated RhoB is associated with UC and contributes to its development by influencing cell signaling and the gut microbiome.
  • Targeting RhoB may offer a novel therapeutic strategy for UC.
  • RhoB shows potential as a diagnostic biomarker for UC.