<p>Chitinases and Chitinase-Like Proteins in Obstructive Lung Diseases – Current Concepts and Potential Applications</p>

Abstract

Chitinases, enzymes that cleave chitin's chain to low molecular weight chitooligomers, are widely distributed in nature. Mammalian chitinases belong to the 18-glycosyl-hydrolase family and can be divided into two groups: true chitinases with enzymatic activity (AMCase and chitotriosidase) and chitinase-like proteins (CLPs) molecules which can bind to chitin or chitooligosaccharides but lack enzymatic activity (eg, YKL-40). Chitinases are thought to be part of an innate immunity against chitin-containing parasites and fungal infections. Both groups of these hydrolases are lately evaluated also as chemical mediators or biomarkers involved in airway inflammation and fibrosis. The aim of this article is to present the current knowledge on the potential role of human chitinases and CLPs in the pathogenesis, diagnosis, and course of obstructive lung diseases. We also assessed the potential role of chitinase and CLPs inhibitors as therapeutic targets in chronic obstructive pulmonary disease and asthma.

Identification of Serum Prognostic Biomarkers of Severe&nbsp;COVID-19 by Quantitative Proteomic Approach

“…Immunohistochemistry also shows that the expression levels of CHI3L1 are enhanced in bronchiolar epithelial cells and alveolar macrophages adjacent to brotic lesions of the patients with IPF, suggesting the possible involvement of CHI3L1 in the brotic process of IPF 21 . These ndings together suggest that CHI3L1 plays an important role in the tissue remodelling of respiratory system in COVID-19 following the massive in ammation and alveolar destruction and local tissue remodelling 22,23 . Therefore, higher levels of CHI3L1 might be associated with the pathogenesis of COVID-19 especially in relevance to pulmonary tissue damage and repair.…”

Airway Epithelial Innate Immunity

“…An important molecular component of both helminths and fungi that signals infection is chitin, which is found in the cuticle and grinder of multiple helminths, and in the cell wall of multiple fungal species (Dickey, 2007;Przysucha et al, 2020). Introduction of chitin into the lungs of mice strongly induces airway epithelial mucous metaplasia and the accumulation of ILC2s and eosinophils (Reese et al, 2007).…”

“…Specifically, lumenal mucus traps larvae in the airway lumen, preventing the completion of the parasite life cycle of migration to the gut. Similarly, chitinases and chitinase-like proteins promote resistance to both parasites and fungi, but can also contribute to the pathophysiology of asthma and other airway diseases (Bigot et al, 2020;Przysucha et al, 2020). The roles of multiple other molecules involved in Type 2 epithelial responses have a similar two-sided character, participating both in resistance to helminths and fungi and in the pathogenesis of non-infectious airway diseases (Hammad and Lambrecht, 2021).…”

“…Neither have these therapies been associated with an increase in airway fungal infection, though whether this is due to the effectiveness of baseline mucociliary clearance, the effectiveness of Type 3 antifungal immune mechanisms that act in parallel to Type 2 mechanisms, or some other reason, is not clear. Targeting Type 2 effector mechanisms, such as chitinases, MUC5AC, and ClCa (chloride channel accessory) signaling in allergic diseases is also being explored (Keeler et al, 2018;Przysucha et al, 2020), and might be expected to have similar benefit without incurring substantial cost in parasite or fungal defense. By the same line of reasoning but in the opposite direction, augmentation of Type 2 epithelial immune responses would generally not be expected to have therapeutic value in industrialized countries.…”

Occupational Exposure to Gasoline in Gasoline Station Male Attendants Promote M1 Polarization in Macrophages

“…Przysucha et al (2020) reported that, mammals are mainly express chitinases and chitinase-like proteins which are secreted by phagocytes (mainly neutrophils and macrophages). These cells are induced at the sites of in ammation, infection and tissue remodeling.…”