Please use this identifier to cite or link to this item:
Title: HMGB1 is upregulated in the airways in asthma and potentiates airway smooth muscle contraction via TLR4
Authors: Di Candia, Leonarda
Gomez, Edith
Venereau, Emilie
Chachi, Latifa
Kaur, Davinder
Bianchi, Marco E.
Challiss, R. A. John
Brightling, Christopher E.
Saunders, Ruth M.
First Published: 1-Mar-2017
Publisher: Elsevier for American Academy of Allergy, Asthma and Immunology, Mosby
Citation: Journal of Allergy and Clinical Immunology, 2017
Abstract: [First paragraph] Asthma is characterized by variable airflow obstruction, airway hyperresponsiveness, and inflammation. Airway smooth muscle (ASM) contributes to asthma pathophysiology via hypercontractility, increased mass, and inflammatory mediator release.1 Clinical studies and animal models demonstrate a role for high-mobility group box 1 (HMGB1) and its receptors in airway inflammation and asthma.2 ; 3 HMGB1's activity and receptor interactions is determined by its redox state, with oxidation rendering HMGB1 inactive.4 We have investigated the redox state of airway HMGB1 and the role of HMGB1 in ASM function.
DOI Link: 10.1016/j.jaci.2016.11.049
ISSN: 0091-6749
eISSN: 1097-6825
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright 2017 The Authors. Published by Elsevier, Inc. on behalf of the American Academy of Allergy, Asthma & Immunology. This is an open access article under the CC BY license (
Description: In Press, Corrected Proof
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

Files in This Item:
File Description SizeFormat 
1-s2.0-S0091674917300477-main.pdfPublished (publisher PDF)2.46 MBAdobe PDFView/Open

Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.