title: Beneficial effect of low-level laser therapy in acute lung injury after i-I/R is dependent on the secretion of IL-10 and independent of the TLR/MyD88 signaling.
abstract: The use of low-level laser for lung inflammation treatment has been evidenced in animal studies as well as clinical trials. The laser action mechanism seems to involve downregulation of neutrophil chemoattractants and transcription factors. Innate immune responses against microorganisms may be mediated by toll-like receptors (TLR). Intestinal ischemia and reperfusion (i-I/R) lead to bacterial product translocation, such as endotoxin, which consequently activates TLRs leading to intestinal and lung inflammation after gut trauma. Thus, the target of this study was to investigate the role of TLR activation in the laser (660 nm, 30 mW, 67.5 J/cm2, 0.375 mW/cm2, 5.4 J, 180 s, and spot size with 0.08 cm2) effect applied in contact with the skin on axillary lymph node in lung inflammation induced by i-I/R through a signaling adaptor protein known as myeloid differentiation factor 88 (MyD88). It is a quantitative, experimental, and laboratory research using the C57Bl/6 and MyD88-/-mice (n = 6 mice for experimental group). Statistical differences were evaluated by ANOVA and the Tukey-Kramer multiple comparisons test to determine differences among groups. In order to understand how the absence of MyD88 can interfere in the laser effect on lung inflammation, MyD88-/-mice were treated or not with laser and subjected to occlusion of the superior mesenteric artery (45 min) followed by intestinal reperfusion (4 h). In summary, the laser decreased the MPO activity and the lung vascular permeability, thickened the alveolar septa, reduced both the edema and the alveolar hemorrhage, as well as significantly decreased neutrophils infiltration in MyD88-deficient mice as well in wild-type mice. It noted a downregulation in chemokine IL-8 production as well as a cytokine IL-10 upregulation in these animals. The results also evidenced that in absence of IL-10, the laser effect is reversed. Based on these results, we suggest that the beneficial effect of laser in acute lung injury after i-I/R is dependent on the secretion of IL-10 and independent of the TLR/MyD88 signaling.
authors.affiliation: Department of Science and Technology, Federal University of São Paulo - UNIFESP, São José dos Campos, SP, Brazil.
authors.forename: J L
authors.initials: JL
authors.lastname: Carvalho
authors.affiliation: Laboratory of Pulmonary Immunology and Exercise, University Nove de Julho - UNINOVE, São José dos Campos, Brazil.
authors.forename: A
authors.initials: A
authors.lastname: Britto
authors.affiliation: Laboratory of Pulmonary Immunology and Exercise, University Nove de Julho - UNINOVE, São José dos Campos, Brazil.
authors.forename: A P Ligeiro
authors.initials: AP
authors.lastname: de Oliveira
authors.affiliation: Laboratory of Immunopharmacology, Oswaldo Cruz Foundation - FIOCRUZ, Rio de Janeiro, RJ, Brazil.
authors.forename: H
authors.initials: H
authors.lastname: Castro-Faria-Neto
authors.affiliation: Department of Science and Technology, Federal University of São Paulo - UNIFESP, São José dos Campos, SP, Brazil.
authors.forename: R
authors.initials: R
authors.lastname: Albertini
authors.affiliation: Department of Science and Technology, Federal University of São Paulo - UNIFESP, São José dos Campos, SP, Brazil.
authors.forename: E
authors.initials: E
authors.lastname: Anatriello
authors.affiliation: Department of Science and Technology, Federal University of São Paulo - UNIFESP, São José dos Campos, SP, Brazil. flavio.aimbire@unifesp.br.|Federal University of São Paulo - UNIFESP, Institute of Science and Technology, Rua Talim, no. 330 - Vila Nair, CEP: 12231-280, São José dos Campos, SP, Brazil. flavio.aimbire@unifesp.br.
authors.forename: F
authors.initials: F
authors.lastname: Aimbire
mesh_terms: D055371:Acute Lung Injury / Q000150:complications / Q000235:genetics / Q000532:radiotherapy*; D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism*; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D007422:Intestines / Q000098:blood supply* / Q000473:pathology; D028022:Low-Level Light Therapy / Q000379:methods*; D008168:Lung / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D008810:Mice, Inbred C57BL; D055806:Microvessels / Q000187:drug effects / Q000473:pathology; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D008926:Plicamycin / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D015398:Signal Transduction / Q000187:drug effects; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D016209:Interleukin-8; D053594:Myeloid Differentiation Factor 88; D012333:RNA, Messenger; D051193:Toll-Like Receptors; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; D009195:Peroxidase; D008926:Plicamycin
keywords: Intestinal ischemia–reperfusion; Laser therapy; Lung inflammation; Myeloid differentiation gene 88