NDLI: Distinct TLR-mediated pathways regulate house dust mite-induced allergic disease in the upper and lower airways.

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Distinct TLR-mediated pathways regulate house dust mite-induced allergic disease in the upper and lower airways.

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Distinct TLR-mediated pathways regulate house dust mite-induced allergic disease in the upper and lower airways.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ryu, Ji-Hwan Yoo, Jung-Yeon Kim, Min-Ji Hwang, Sang-Gyu Ahn, Kwang Chul Ryu, Jae-Chan Choi, Mi-Kyung Joo, Jung Hee Kim, Chang-Hoon Lee, Sang-Nam Lee, Won-Jae Kim, Jaesang Shin, Dong Min Kweon, Mi-Na Bae, Yun Soo Yoon, Joo-Heon
Description	Author Affiliation: Ryu JH ( Research Center for Human Natural Defense System, Yonsei University College of Medicine, Seoul, Korea.)
Abstract	BACKGROUND: Allergic rhinitis (AR) and asthma are 2 entities of allergic airway diseases that frequently occur together, which is referred to as united airways. In contrast to this general concept, we hypothesized that innate immunity of the upper and lower airways is respectively distinctive, because the immunologic conditions of the nasal and lung mucosa as well as the functions of the immune cells within their epithelia are different. OBJECTIVE: We wanted to identify distinctive mechanisms of innate immunity in the nose and lung mucosa, which are responsible for house dust mite (HDM)-induced AR and allergic asthma (AA), respectively. METHODS: We constructed a mouse model of AR or AA induced by sensitization and consequent provocation with HDM extracts. RESULTS: HDM-derived ß-glucans, rather than LPS, were proven to be essential to activating innate immunity in the nasal mucosa and triggering AR, which depended on Toll-like receptor 2 (TLR2), but not on TLR4; however, the LPS/TLR4 signaling axis, rather than ß-glucans/TLR2, was critical to HDM-induced AA. These differences were attributed to the specific role of ß-glucans and LPS in inducing the surface expression of TLR2 and TLR4 and their translocation to lipid rafts in nasal and bronchial epithelial cells, respectively. We also showed that dual oxidase 2-generated reactive oxygen species mediate both ß-glucan-induced TLR2 activation and LPS-induced TLR4 activation. CONCLUSIONS: We describe a novel finding of distinctive innate immunity of the nose and lungs, respectively, which trigger AR and AA, by showing the critical role of HDM-induced TLR activation via dual oxidase 2-mediated reactive oxygen species.
File Format	HTM / HTML
ISSN	00916749
e-ISSN	10976825
Journal	Journal of Allergy and Clinical Immunology
Issue Number	2
Volume Number	131
Language	English
Publisher	Elsevier
Publisher Date	2013-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Immunology Hypersensitivity Immunology Lung Nasal Mucosa Pyroglyphidae Respiratory System Toll-like Receptor 2 Metabolism Toll-like Receptor 4 Animals Asthma Epithelial Cells Immunity, Innate Lipopolysaccharides Mice Nadph Oxidase Reactive Oxygen Species Respiratory Mucosa Rhinitis, Allergic Rhinitis, Allergic, Perennial Beta-glucans Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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