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|Title:||HMGB1 is upregulated in the airways in asthma and potentiates airway smooth muscle contraction via TLR4|
|Authors:||Di Candia, Leonarda|
Bianchi, Marco E.
Challiss, R. A. John
Brightling, Christopher E.
Saunders, Ruth M.
|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.|
|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 (http://creativecommons.org/licenses/by/4.0/).|
|Description:||In Press, Corrected Proof|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
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|1-s2.0-S0091674917300477-main.pdf||Published (publisher PDF)||2.46 MB||Adobe PDF||View/Open|
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