NDLI: Alternatively spliced myeloid differentiation protein-2 inhibits TLR4-mediated lung inflammation.

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Alternatively spliced myeloid differentiation protein-2 inhibits TLR4-mediated lung inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jones, Heather D. Crother, Timothy R. Chen, Shuang Shimada, Kenichi Tumurkhuu, Gantsetseg Arditi, Moshe Dagvadorj, Jargalsaikhan
Description	Author Affiliation: Tumurkhuu G ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048); Dagvadorj J ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048); Jones HD ( Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.); Chen S ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048); Shimada K ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048); Crother TR ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048); Arditi M ( Division of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA 90048)
Abstract	We previously identified a novel alternatively spliced isoform of human myeloid differentiation protein-2 (MD-2s) that competitively inhibits binding of MD-2 to TLR4 in vitro. In this study, we investigated the protective role of MD-2s in LPS-induced acute lung injury by delivering intratracheally an adenovirus construct that expressed MD-2s (Ad-MD-2s). After adenovirus-mediated gene transfer, MD-2s was strongly expressed in lung epithelial cells and readily detected in bronchoalveolar lavage fluid. Compared to adenovirus serotype 5 containing an empty vector lacking a transgene control mice, Ad-MD-2s delivery resulted in significantly less LPS-induced inflammation in the lungs, including less protein leakage, cell recruitment, and expression of proinflammatory cytokines and chemokines, such as IL-6, keratinocyte chemoattractant, and MIP-2. Bronchoalveolar lavage fluid from Ad-MD-2s mice transferred into lungs of naive mice before intratracheal LPS challenge diminished proinflammatory cytokine levels. As house dust mite (HDM) sensitization is dependent on TLR4 and HDM Der p 2, a structural homolog of MD-2, we also investigated the effect of MD-2s on HDM-induced allergic airway inflammation. Ad-MD-2s given before HDM sensitization significantly inhibited subsequent allergic airway inflammation after HDM challenge, including reductions in eosinophils, goblet cell hyperplasia, and IL-5 levels. Our study indicates that the alternatively spliced short isoform of human MD-2 could be a potential therapeutic candidate to treat human diseases induced or exacerbated by TLR4 signaling, such as Gram-negative bacterial endotoxin-induced lung injury and HDM-triggered allergic lung inflammation.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1402123
Journal	The Journal of Immunology
Issue Number	4
Volume Number	194
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Lymphocyte Antigen 96 Immunology Pneumonia Genetics Acute Lung Injury Alternative Splicing Animals Blotting, Western Disease Models, Animal Flow Cytometry Hypersensitivity Immunohistochemistry Mice Mice, Inbred C57bl Mice, Transgenic Protein Isoforms Real-time Polymerase Chain Reaction Toll-like Receptor 4 Transfection Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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