NDLI: Bacillus-derived poly-Î³-glutamic acid attenuates allergic airway inflammation through a Toll-like receptor-4-dependent pathway in a murine model of asthma.

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Bacillus-derived poly-Î³-glutamic acid attenuates allergic airway inflammation through a Toll-like receptor-4-dependent pathway in a murine model of asthma.

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Bacillus-derived poly-Î³-glutamic acid attenuates allergic airway inflammation through a Toll-like receptor-4-dependent pathway in a murine model of asthma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, K. Kim, S-H Yoon, H. J. Paik, D. J. Kim, J. M. Youn, J.
Description	Author Affiliation: Lee K ( Department of Biomedical Sciences, College of Medicine, Hanyang University, Seoul, Korea.)
Abstract	BACKGROUND: Asthma is an inflammatory disease of the airways that is mediated by Th2 responses. Poly-Î³-glutamic acid (Î³-PGA) is an extracellular polymeric compound that is synthesized by Bacillus cells. Previously, we found that Î³-PGA promoted Th1 cell development in a manner dependent on antigen-presenting cells, but inhibited Th2 cell development. OBJECTIVE: To investigate the effect of Î³-PGA on dendritic cells (DCs), and its potential for treating Th2-mediated allergic asthma. METHODS: Wild-type, Toll-like receptor (TLR)-2 deficient, and TLR-4-defective mice were used. DCs derived from the bone marrow and extracted from the lung were stimulated with Î³-PGA and assayed for the expression of signalling molecules, costimulatory molecules, and cytokines. Mice were sensitized and challenged with ovalbumin (OVA) to induce asthma. They were repeatedly injected intranasally with Î³-PGA before and during the challenge period, and inflammation and structural remodelling of the airways were examined. RESULTS: Î³-PGA selectively signalled conventional DCs to activate NF-κB and mitogen-activated protein kinase, leading to the up-regulation of CD86, CD40, and IL-12, but not IL-10 and IL-6. These effects of Î³-PGA were dependent on TLR-4 and independent of TLR-2. Importantly, the intranasal administration of Î³-PGA to OVA-sensitized/challenged mice reduced the airway hyperresponsiveness and allergic inflammation such as leucocyte influx, goblet cell hyperplasia, eosinophilia, and Th2 cytokine production. In addition to lowered IgE titres, the treatment of mice with Î³-PGA significantly reduced the multiplication and Th2 polarization of mediastinal lymph node T cells upon allergen-specific restimulation. These anti-asthmatic effects of Î³-PGA were also abolished in TLR-4-defective mice. CONCLUSIONS AND CLINICAL RELEVANCE: Our data indicate that Î³-PGA activates DCs to favour Th1 cell induction through a TLR-4-dependent pathway and alleviates pathologic symptoms in a Th2-biased asthmatic model. These findings highlight the potential of Î³-PGA for the treatment of asthma and other allergic disease in which Th2 polarization plays an important role.
File Format	HTM / HTML
ISSN	09547894
Issue Number	8
Volume Number	41
e-ISSN	13652222
Journal	Clinical & Experimental Allergy
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2011-08-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Immunology Asthma Drug Therapy Bacillus Chemistry Bronchial Hyperreactivity Disease Models, Animal Inflammation Polyglutamic Acid Pharmacology Toll-like Receptor 4 Immunology Animals Dendritic Cells Drug Effects Mice Mice, Congenic Mice, Inbred Balb C Mice, Inbred C3h Mice, Inbred C57bl Mice, Inbred Nod Th2 Cells Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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