Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease

Int J Mol Sci. 2023 Dec 22;25(1):202. doi: 10.3390/ijms25010202.

Abstract

Inflammatory bowel disease (IBD) is a collective term for two diseases: ulcerative colitis (UC) and Crohn's disease (CD). There are many factors, e.g., genetic, environmental and immunological, that increase the likelihood of these diseases. Indicators of IBDs include extracellular matrix metalloproteinases (MMPs). The aim of this review is to present data on the role of selected cytokines and metalloproteinases in IBD. In recent years, more and more transcriptomic studies are emerging. These studies are improving the characterization of the cytokine microenvironment inside inflamed tissue. It is observed that the levels of several cytokines are consistently increased in inflamed tissue in IBD, both in UC and CD. This review shows that MMPs play a major role in the pathology of inflammatory processes, cancer, and IBD. IBD-associated inflammation is associated with increased expression of MMPs and reduced ability of tissue inhibitors of metalloproteinases (TIMPs) to inhibit their action. In IBD patients in tissues that are inflamed, MMPs are produced in excess and TIMP activity is not sufficient to block MMPs. This review is based on our personal selection of the literature that was retrieved by a selective search in PubMed using the terms "Inflammatory bowel disease" and "pathogenesis of Inflammatory bowel diseases" that includes systematic reviews, meta-analyses, and clinical trials. The involvement of the immune system in the pathophysiology of IBD is reviewed in terms of the role of the cytokines and metalloproteinases involved.

Keywords: CD; IBD; MMPs; UC; cytokines; inflammatory bowel disease; metalloproteinases.

Publication types

  • Review

MeSH terms

  • Colitis, Ulcerative*
  • Crohn Disease*
  • Cytokines
  • Humans
  • Inflammatory Bowel Diseases* / genetics
  • Matrix Metalloproteinases / genetics

Substances

  • Cytokines
  • Matrix Metalloproteinases

Grants and funding

This research received no external funding.