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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome

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Author(s):
de Lima, Flavia Mafra [1] ; Moreira, Leonardo M. [2] ; Villaverde, A. B. [3] ; Albertini, Regiane [4] ; Castro-Faria-Neto, Hugo C. [5] ; Aimbire, Flavio [6]
Total Authors: 6
Affiliation:
[1] Res & Dev Inst IP&D, Sao Jose Dos Campos, SP - Brazil
[2] Dept Biosyst Engn, BR-36301160 Sao Joao Del Rei, MG - Brazil
[3] Unicastelo, Inst Biomed Engn, BR-12247004 Sao Jose Dos Campos, SP - Brazil
[4] Ctr Univ Nove Julho Uninove, Rehabil Sci Dept, Sao Paulo, SP - Brazil
[5] Fiocruz MS, Lab Immunopharmacol, BR-21045900 Rio De Janeiro - Brazil
[6] Fed Univ Sao Paulo UNIFESP, Dept Sci & Technol, Sao Jose Dos Campos, SP - Brazil
Total Affiliations: 6
Document type: Journal article
Source: Lasers in Medical Science; v. 26, n. 3, p. 389-400, MAY 2011.
Web of Science Citations: 15
Abstract

The aim of this work was to investigate if the low-level laser therapy (LLLT) on acute lung inflammation (ALI) induced by lipopolysaccharide (LPS) is linked to tumor necrosis factor (TNF) in alveolar macrophages (AM) from bronchoalveolar lavage fluid (BALF) of mice. LLLT has been reported to actuate positively for relieving the late and early symptoms of airway and lung inflammation. It is not known if the increased TNF mRNA expression and dysfunction of cAMP generation observed in ALI can be influenced by LLLT. For in vivo studies, Balb/c mice (n = 5 for group) received LPS inhalation or TNF intra nasal instillation and 3 h after LPS or TNF-alpha, leukocytes in BALF were analyzed. LLLT administered perpendicularly to a point in the middle of the dissected bronchi with a wavelength of 660 nm and a dose of 4.5 J/cm(2). The mice were irradiated 15 min after ALI induction. In vitro AM from mice were cultured for analyses of TNF mRNA expression and protein and adenosine3':5'-cyclic monophosphate (cAMP) levels. One hour after LPS, the TNF and cAMP levels in AM were measured by ELISA. RT-PCR was used to measure TNF mRNA in AM. The LLLT was inefficient in potentiating the rolipram effect in presence of a TNF synthesis inhibitor. LLLT attenuated the neutrophil influx and TNF in BALF. In AM, the laser increased the cAMP and reduced the TNF-alpha mRNA. LLLT increases indirectly the cAMP in AM by a TNF-dependent mechanism. (AU)

FAPESP's process: 08/08048-4 - Study of anti-inflammatory action of low level laser therapy on bronchial reactivity and lung inflammation induced by intestinal reperfusion ischemia in rats
Grantee:Flávia Mafra de Lima
Support Opportunities: Scholarships in Brazil - Master