Low-level laser therapy inhibits bronchoconstriction, Th2 inflammation and airway remodeling in allergic asthma

Low-level laser therapy inhibits bronchoconstriction, Th2 inflammation and airway remodeling in allergic asthma

Author Silva, Vanessa R. Google Scholar
Marcondes, P. Autor UNIFESP Google Scholar
Silva, M. Google Scholar
Villaverde, Antonio B. Google Scholar
Castro-Faria-Neto, Hugo C. Google Scholar
Vieira, Rodolfo P. Google Scholar
Aimbire, Flavio Autor UNIFESP Google Scholar
Oliveira, Ana Paula L. de Google Scholar
Institution Nove de Julho Univ UNINOVE
Universidade Federal de São Paulo (UNIFESP)
Fiocruz MS
Abstract Low-level laser therapy (LLLT) controls bronchial hyperresponsiveness (BHR) associated with increased RhoA expression as well as pro-inflammatory mediators associated with NF-kB in acute lung inflammation. Herein, we explore if LLLT can reduce both BHR and Th2 cytokines in allergic asthma. Mice were studied for bronchial reactivity and lung inflammation after antigen challenge. BHR was measured through dose-response curves to acetylcholine. Some animals were pretreated with a RhoA inhibitor before the antigen. LLLT (660 nm, 30 mW and 5.4 J) was applied on the skin over the right upper bronchus and two irradiation protocols were used. Reduction of BHR post LLLT coincided with lower RhoA expression in bronchial muscle as well as reduction in eosinophils and eotaxin. LLLT also diminished ICAM expression and Th2 cytokines as well as signal transducer and activator of transduction 6 (STAT6) levels in lungs from challenged mice. Our results demonstrated that LLLT reduced BHR via RhoA and lessened allergic lung inflammation via STAT6. (C) 2014 Elsevier B.V. All rights reserved.
Keywords Allergy
Airway hyperresponsiveness
Laser therapy
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Grant number FAPESP: 2008/08838-5
Date 2014-04-01
Published in Respiratory Physiology & Neurobiology. Amsterdam: Elsevier B.V., v. 194, p. 37-48, 2014.
ISSN 1569-9048 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 37-48
Origin http://dx.doi.org/10.1016/j.resp.2014.01.008
Access rights Closed access
Type Article
Web of Science ID WOS:000334002400007
URI http://repositorio.unifesp.br/handle/11600/37626

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