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HMGB1 is upregulated in the airways in asthma and potentiates airway smooth muscle contraction via TLR4

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journal contribution
posted on 10.03.2017, 09:46 by Leonarda Di Candia, Edith Gomez, Emilie Venereau, Latifa Chachi, Davinder Kaur, Marco E. Bianchi, R. A. John Challiss, Christopher E. Brightling, Ruth M. Saunders
[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.

Funding

Open Access funded by Wellcome Trust

History

Citation

Journal of Allergy and Clinical Immunology, 2017

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine/Department of Infection, Immunity and Inflammation

Version

VoR (Version of Record)

Published in

Journal of Allergy and Clinical Immunology

Publisher

Elsevier for American Academy of Allergy, Asthma and Immunology, Mosby

issn

0091-6749

eissn

1097-6825

Copyright date

2017

Available date

10/03/2017

Publisher version

http://www.sciencedirect.com/science/article/pii/S0091674917300477

Notes

In Press, Corrected Proof

Language

en

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