Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation-Reference-Cited by-同舟云学术

Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation

Published:2004-06-11 Issue:5677 Volume:304 Page:1678-1682
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Zhu Zhou¹²³⁴,Zheng Tao¹²³⁴,Homer Robert J.¹²³⁴,Kim Yoon-Keun¹²³⁴,Chen Ning Yuan¹²³⁴,Cohn Lauren¹²³⁴,Hamid Qutayba¹²³⁴,Elias Jack A.¹²³⁴

Affiliation:

1. Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, Department of Internal Medicine, 300 Cedar Street, TAC S-441, New Haven, CT 06520–8057, USA.

2. Department of Pathology, Yale University School of Medicine, 310 Cedar Street, 108 LH, New Haven, CT 06520–8057, USA.

3. Pathology and Laboratory Medicine Service, VA-CT Health Care System, 950 Campbell Avenue, West Haven, CT 06516, USA.

4. Meakins-Christie Laboratories, 3626 Saint Urbain, McGill University, Montreal, Quebec, H2X 2P2, Canada.

Abstract

Chitin is a surface component of parasites and insects, and chitinases are induced in lower life forms during infections with these agents. Although chitin itself does not exist in humans, chitinases are present in the human genome. We show here that acidic mammalian chitinase (AMCase) is induced via a T helper-2 (Th2)–specific, interleukin-13 (IL-13)–mediated pathway in epithelial cells and macrophages in an aeroallergen asthma model and expressed in exaggerated quantities in human asthma. AMCase neutralization ameliorated Th2 inflammation and airway hyperresponsiveness, in part by inhibiting IL-13 pathway activation and chemokine induction. AMCase may thus be an important mediator of IL-13–induced responses in Th2-dominated disorders such as asthma.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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