Chitinases and chitinase-like proteins in TH2 inflammation and asthma

• Published in: Journal of allergy and clinical immunology Vol. 116; no. 3; pp. 497 - 500
• Main Authors: ELIAS, Jack A, HOMER, Robert J, HAMID, Qutayba, CHUN GEUN LEE
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier 01.09.2005; Elsevier Limited
• Subjects: Arthritis; Biological and medical sciences; Biology; Cell growth; Chemokines; Chitinase; Chromosomes; Enzymes; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Heparan sulfate; Immunopathology; Infections; Mammals; Medical sciences; Parasites; Pathogenesis; Proteins; Chitinase; breast regiesstion protem 39. TH2 inflammation; acidic mammalian chitinase; Immunology; T-Lymphocyte; Bronchus disease; Th2 lymphocyte; Obstructive pulmonary disease; Mammary gland; Immunopathology; Lung disease; Respiratory disease; Enzyme; Cytokine; Inflammation; Interleukin 13; IL-13; Protein; Asthma; Vertebrata; Mammalia; Glycosidases; Breast; Hydrolases; O-Glycosidases
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/j.jaci.2005.06.028

Chitin is the second most abundant biopolymer in nature, where it protects crustaceans, parasites, fungi, and other pathogens from the adverse effects of their environments, hosts, or both. Because chitin does not exist in mammals, it had been assumed that the chitinases that degrade it are also restricted to lower life forms. However, chitinases and chitinase-like proteins have recently been noted in mice and human subjects. The prototypic chitinase, acidic mammalian chitinase, was also noted to be induced during TH2 inflammation through an IL-13-dependent mechanism. It was also shown to play an important role in the pathogenesis of TH2 inflammation and IL-13 effector pathway activation and demonstrated to be expressed in an exaggerated fashion in human asthmatic tissues. The finding that chitinases contribute to host antiparasite responses and asthmatic TH2 inflammation support the concept that asthma might be a parasite-independent antiparasite response.