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

Autor(es)

Silva, Vanessa R. ^[1] ; Marcondes, P. ^[2] ; Silva, M. ^[1] ; Villaverde, Antonio B. ^[3] ; Castro-Faria-Neto, Hugo C. ^[4] ; Vieira, Rodolfo P. ^[1] ; Aimbire, Flavio ^[2] ; de Oliveira, Ana Paula L. ^[1]

Afiliação do(s) autor(es)

^[1] Nove de Julho Univ UNINOVE, Lab Pulm & Exercise Immunol LABPEI, Sao Paulo - Brazil

^[2] Univ Fed Sao Paulo, Dept Sci & Technol, Sao Jose Dos Campos, SP - Brazil

^[3] UNICASTELO, Inst Biomed Engn, Sao Jose Dos Campos, SP - Brazil

^[4] Fiocruz MS, IOC, Lab Immunopharmacol, Rio De Janeiro, RJ - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Respiratory Physiology & Neurobiology; v. 194, p. 37-48, APR 1 2014.
• Citações Web of Science: 16

Resumo

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. (AU)

• Processo FAPESP: 08/08838-5 - Estudo do mecanismo de ação antiinflamatória do laser de baixa potência em modelo experimental de inflamação pulmonar alérgica e sistêmica
• Beneficiário: Flávio Aimbire Soares de Carvalho
• Modalidade de apoio: Auxílio à Pesquisa - Regular