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
Autor: | Elen Anatriello, Aurileia Britto, Regiane Albertini, A. P. Ligeiro de Oliveira, Flavio Aimbire, Jose Maria La Fuente Carvalho, Hugo C. Castro-Faria-Neto |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Chemokine medicine.medical_treatment Acute Lung Injury Inflammation Dermatology Pharmacology Lung injury 03 medical and health sciences Downregulation and upregulation Medicine Animals RNA Messenger Low-Level Light Therapy Lung Low level laser therapy Peroxidase biology business.industry Interleukin-8 Toll-Like Receptors Plicamycin Intercellular Adhesion Molecule-1 Interleukin-10 Intestines Mice Inbred C57BL Interleukin 10 030104 developmental biology medicine.anatomical_structure Cytokine Gene Expression Regulation Reperfusion Injury Immunology Microvessels Myeloid Differentiation Factor 88 biology.protein Surgery medicine.symptom business Signal Transduction |
Zdroj: | Lasers in medical science. 32(2) |
ISSN: | 1435-604X |
Popis: | 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. |
Databáze: | OpenAIRE |
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