NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease

Author:

Zhou Feng12,Zhang Guo Dong3,Tan Yang14,Hu Shi An15,Tang Qun67,Pei Gang62ORCID

Affiliation:

1. School of Pharmacy, Hunan University of Chinese Medicine, Changsha, China

2. Key Laboratory of Modern Research of TCM, Education Department of Hunan Province, Changsha, China

3. Ningxia Medical University, Ningxia, China

4. Science and Technology Innovation Center/State Key Laboratory Breeding Base of Chinese Medicine Powder and Innovative Medicine, Hunan University of Chinese Medicine, Changsha, China

5. Hunan Provincial Key Laboratory of TCM Prevention and Treatment of Depression Diseases, Changsha, China

6. School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China

7. Medical School, Hunan University of Chinese Medicine, Changsha, China

Abstract

Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease that involves host genetics, the microbiome, and inflammatory responses. The current consensus is that the disruption of the intestinal mucosal barrier is the core pathogenesis of IBD, including intestinal microbial factors, abnormal immune responses, and impaired intestinal mucosal barrier. Cumulative data show that nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are dominant mediators in maintaining the homeostasis of the intestinal mucosal barrier, which play critical roles in sensing the commensal microbiota, maintaining homeostasis, and regulating intestinal inflammation. Blocking NLRs inflammasome activation by botanicals may be a promising way to prevent IBD progression. In this review, we systematically introduce the multiple roles of NLRs in regulating intestinal mucosal barrier homeostasis and focus on summarizing the activities and potential mechanisms of natural products against IBD. Aiming to propose new directions on the pathogenesis and precise treatment of IBD

Publisher

SAGE Publications

Subject

Gastroenterology

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