» Articles » PMID: 33381598

Alleviates Colitis Via the IL-22/Occludin Signal Pathway

Overview
Journal Biomed Res Int
Publisher Wiley
Date 2020 Dec 31
PMID 33381598
Citations 3
Authors
Affiliations
Soon will be listed here.
Abstract

Ulcerative colitis (UC) is the most common inflammatory bowel disease, and its incidence has increased in recent years. Recent clinical and experimental data indicate that gut microbiota plays a pivotal role in the pathogenesis of UC. establishes a stable and persistent colonization in the gastrointestinal tract without apparent pathogenicity to gastrointestinal or extragastrointestinal tissues. However, the detailed effects of on the gastrointestinal tissue remain unknown. The primary aim of this study is to investigate the effects of () on development of colitis induced by dextran sodium sulfate (DSS) and the underlying molecular mechanism. The results suggested that significantly improved colitis symptoms-including weight loss, disease activity index, colon length, and histopathological changes in the colon caused by DSS-and alleviated the reduced expression of interleukin-22 and occludin in the colonic tissue due to DSS administration. Furthermore, the absence of IL-22 completely prevented from alleviating colitis and significantly decreased the levels of occludin, an important downstream effector protein of IL-22. These findings suggest that ameliorates ulcerative colitis induced by DSS via the IL-22/occludin signal pathway.

Citing Articles

Causes Persistent Subclinical Infection and Elicits Innate and Adaptive Immune Responses in C57BL/6J, BALB/cJ and J:ARC(S) Mice Following Exposure to Shedding Mice.

Mishkin N, Carrasco S, Palillo M, Momtsios P, Woods C, Henderson K bioRxiv. 2024; .

PMID: 39071441 PMC: 11275779. DOI: 10.1101/2024.07.16.603732.


Therapeutic Effects of on Experimental DSS-Induced Colitis Mouse Model.

Almo M, Sousa I, Olinto V, Pinhate S, Jivago J, de Sousa D Microorganisms. 2023; 11(11).

PMID: 38004805 PMC: 10672878. DOI: 10.3390/microorganisms11112793.


IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis.

Nong H, Yuan H, Lin Y, Chen S, Li Y, Luo Z Mol Cell Biochem. 2023; 479(6):1443-1450.

PMID: 37440121 DOI: 10.1007/s11010-023-04806-z.

References
1.
Zhao D, Cai C, Zheng Q, Jin S, Song D, Shen J . Vancomycin pre-treatment impairs tissue healing in experimental colitis: Importance of innate lymphoid cells. Biochem Biophys Res Commun. 2016; 483(1):237-244. DOI: 10.1016/j.bbrc.2016.12.160. View

2.
Zhang Y, Zhao X, Zhu Y, Ma J, Ma H, Zhang H . Probiotic Mixture Protects Dextran Sulfate Sodium-Induced Colitis by Altering Tight Junction Protein Expressions and Increasing Tregs. Mediators Inflamm. 2018; 2018:9416391. PMC: 5925202. DOI: 10.1155/2018/9416391. View

3.
Van Itallie C, Fanning A, Holmes J, Anderson J . Occludin is required for cytokine-induced regulation of tight junction barriers. J Cell Sci. 2010; 123(Pt 16):2844-52. PMC: 2915885. DOI: 10.1242/jcs.065581. View

4.
Wang L, Zhu C, Zhang T, Tian Q, Zhang N, Morrison S . Nonpathogenic Colonization with Chlamydia in the Gastrointestinal Tract as Oral Vaccination for Inducing Transmucosal Protection. Infect Immun. 2017; 86(2). PMC: 5778366. DOI: 10.1128/IAI.00630-17. View

5.
Spalinger M, Schmidt T, Schwarzfischer M, Hering L, Atrott K, Lang S . Protein tyrosine phosphatase non-receptor type 22 modulates colitis in a microbiota-dependent manner. J Clin Invest. 2019; 129(6):2527-2541. PMC: 6546451. DOI: 10.1172/JCI123263. View