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Review
. 2023 Dec 22;25(1):202.
doi: 10.3390/ijms25010202.

Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease

Affiliations
Review

Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease

Barbara Sosna et al. Int J Mol Sci. .

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.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Scoring system for assessment of UC activity [1,2,3,4,5,6,7].
Figure 2
Figure 2
Selected endoscopic and microscopic upper gastrointestinal signs in UC.
Figure 3
Figure 3
Factors affecting the development of IBD.
Figure 4
Figure 4
Scheme of cytokines production. APC: anaphase-promoting complex, CSF: colony stimulating factor, EBI: Epstein–Barr virus-induced gene, IFN: interferon, IL: interleukin, LIF: leukemia inducing factor, LT: lymphotoxin, OSM: oncostatin M, TGF: transforming growth factor, TL1A: TNF-like cytokine 1A, TCR: T-cell receptor, TNF: tumor necrosis factor, TNFSF: TNF super family member, TSLP: thymic stromal lymphopoetin. Genome-wide association studies have identified several IBD susceptibility loci containing genes encoding cytokines as well as proteins involved in cytokine signaling. Mutations that cause loss of function in genes encoding interleukin-10 (IL-10) and the IL-10 receptor are associated with very early onset IBD [97].
Figure 5
Figure 5
Cytokinases and their interrelations.

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