Abstract

Chitin, after cellulose, the second most abundant biopolymer on earth, is a key component of insects, fungi, and house-dust mites. Lower life forms are endowed with chitinases to defend themselves against chitin-bearing pathogens. Unexpectedly, humans were also found to express chitinases as well as chitinase-like proteins that modulate immune responses. Particularly, increased levels of the chitinase-like protein YKL-40 have been associated with severe asthma, cystic fibrosis, and other inflammatory disease conditions. Here, we summarize and discuss the potential role of chitin, chitinases, and chitinase-like proteins in pediatric lung diseases.

Highlights

  • The role of chitin and chitinases has been firmly established in the field of plant and microbial immunity by demonstrating that host-derived chitinases cleave chitin to protect against invading chitin-bearing pathogens, such as fungi

  • Chitin Chitin, a polymer of N-acetylglucosamine and the second most abundant polysaccharide in nature following cellulose, is an essential component of fungi, house-dust mites, exoskeletons of crabs, shrimp and insects, parasitic nematodes, and digestive tracts of many insects [1]. Chitin protects these microbes from their environment, and its turnover is regulated by biosynthesis and degradation through endogenous chitinases

  • This study showed that YKL-40 serum levels were mainly increased in adult patients with severe asthma and correlated with disease severity and airway remodeling

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Summary

Introduction

The role of chitin and chitinases has been firmly established in the field of plant and microbial immunity by demonstrating that host-derived chitinases cleave chitin to protect against invading chitin-bearing pathogens, such as fungi. Chitinase-like proteins have been described as dysregulated in a variety of diseases characterized by chronic inflammation and tissue remodeling, yet their potential role for humans has just recently begun to evolve [1,2]. These studies strongly suggest that chitin can contribute to the development of allergic type 2 (Th2) inflammation by activating innate immune cells.

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