Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Recently updated role of Chitinase 3-like 1 on various cell types as a major infuencer of chronic inflammation

Version 1 : Received: 28 February 2024 / Approved: 28 February 2024 / Online: 28 February 2024 (12:49:50 CET)

A peer-reviewed article of this Preprint also exists.

Mizoguchi, E.; Sadanaga, T.; Nanni, L.; Wang, S.; Mizoguchi, A. Recently Updated Role of Chitinase 3-like 1 on Various Cell Types as a Major Influencer of Chronic Inflammation. Cells 2024, 13, 678. Mizoguchi, E.; Sadanaga, T.; Nanni, L.; Wang, S.; Mizoguchi, A. Recently Updated Role of Chitinase 3-like 1 on Various Cell Types as a Major Influencer of Chronic Inflammation. Cells 2024, 13, 678.

Abstract

Chitinase 3-like 1 (also known as CHI3L1 or YKL-40)is a mammalian chitinase that has no enzymatic activity, but has the ability to bind to chitin, the polymer of N-acetylglucosamine (GlcNAc). Chitin is a component of fungi, crustaceans, arthropods including insects and mites, and parasites, but is completely absent from mammals, including humans and mice. In general, chitin-containing organisms produce CHI3L1 to protect the body from exogenous pathogen as well as hostile environments, and it was thought that it has a similar effect in mammals. However, recent studies have revealed that CHI3L1 plays a pro-inflammatory role by inducing anti-apoptotic activity in epithelial cells and macrophages. Under chronic inflammatory conditions such as inflammatory bowel disease and chronic obstructive pulmonary disease, many groups already confirmed that the expression of CHI3L1 is significantly induced on the apical side of epithelial cells, and activates many downstream pathways involved in inflammation and carcinogenesis. In this review article, we will summarize the expression of CHI3L1 under the chronic inflammatory conditions in various disorders and would like to discuss the potential roles of CHI3L1 in those disorders on various cell types.

Keywords

inflammation, pathogenesis, inflammatory bowel disease, asthma, dysbiosis

Subject

Medicine and Pharmacology, Gastroenterology and Hepatology

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