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Journal ArticleDOI

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

TLDR
It is shown 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.
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.

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Citations
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Exploring the full spectrum of macrophage activation.

TL;DR: This Review suggests a new grouping of macrophages based on three different homeostatic activities — host defence, wound healing and immune regulation, and proposes that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation.
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Macrophage plasticity and polarization: in vivo veritas

TL;DR: The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for Macrophage-centered diagnostic and therapeutic strategies.
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Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression

TL;DR: Transcriptome profiling reveals novel molecules and signatures associated with human monocyte-to-macrophage differentiation and polarized activation which may represent candidate targets in pathophysiology.
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Biodegradation, biodistribution and toxicity of chitosan.

TL;DR: Research in this area is reviewed and chitosan's potential to be used as a generally regarded as safe (GRAS) material is critically discussed.
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Macrophages: master regulators of inflammation and fibrosis.

TL;DR: Although collagen-secreting myofibroblasts once were thought of as the master "producers" of fibrosis, this review will illustrate how macrophages function as the Master "regulators" of Fibrosis.
References
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Journal ArticleDOI

Endogenous airway acidification. Implications for asthma pathophysiology.

TL;DR: It is demonstrated that the pH of deaerated exhaled airway vapor condensate is over two log orders lower in patients with acute asthma than in control subjects and normalizes with corticosteroid therapy, and suggested that regulation of airway pH has a previously unsuspected role in asthma pathophysiology.
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Asthma: an epidemic of dysregulated immunity.

TL;DR: This work has shown that in the absence of infections that limit T helper type 2 (TH2)-biased inflammation and asthma, TH2 cells—which are developmentally related to TR cells—develop instead and coordinate the development of asthmatic inflammation.
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Dissection of experimental asthma with DNA microarray analysis identifies arginase in asthma pathogenesis

TL;DR: Analysis of patients with asthma supported the importance of the ability of arginase to regulate generation of NO, polyamines, and collagen, and provided a basis for pharmacologically targeting arginine metabolism in allergic disorders.
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Identification of a novel acidic mammalian chitinase distinct from chitotriosidase

TL;DR: The study has revealed the existence of a chitinolytic enzyme in the gastrointestinal tract and lung that may play a role in digestion and/or defense.
Journal ArticleDOI

Th2 cells and GATA-3 in asthma: new insights into the regulation of airway inflammation

TL;DR: It is now believed that airway inflammation leads to AHR, airway remodeling, and mucus hyperplasia, and it is clear that persistent inflammation is central to the pathogenesis of asthma.
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