Adult Respiratory Distress Syndrome

Lasers Med Sci.  2011 May;26(3):389-400. Epub 2010 Dec 24.

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

de Lima FM, Moreira LM, Villaverde AB, Albertini R, Castro-Faria-Neto HC, Aimbire F.

Source

Research and Development Institute – IP&D, Av. Shishima Hifumi, 2911 – Urbanova, Po Box 12244-00, São José dos Campos, SP, Brazil.

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-?, 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-? mRNA. LLLT increases indirectly the cAMP in AM by a TNF-dependent mechanism.

Lasers Med Sci. 2010 Dec 24. [Epub ahead of print]

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

de Lima FM, Moreira LM, Villaverde AB, Albertini R, Castro-Faria-Neto HC, Aimbire F.

Research and Development Institute – IP&D, Av. Shishima Hifumi, 2911 – Urbanova, Po Box 12244-00, São José dos Campos, SP, Brazil.

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-?, 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-? mRNA. LLLT increases indirectly the cAMP in AM by a TNF-dependent mechanism.

Lasers Surg Med. 2009 Jan;41(1):68-74.

Low level laser therapy (LLLT): attenuation of cholinergic hyperreactivity, beta(2)-adrenergic hyporesponsiveness and TNF-alpha mRNA expression in rat bronchi segments in E. Coli lipo-polysaccharide-induced airway inflammation by a NF-kappaB dependent mechanism.

Mafra de Lima F, Costa MS, Albertini R, Silva JA Jr, Aimbire F.B

Institute of Research and Development (IP&D), São Paulo, Brazil.

BACKGROUND AND OBJECTIVES: It is unknown if the decreased ability to relax airways smooth muscles in asthma and other inflammatory disorders, such as acute respiratory distress syndrome (ARDS), can be influenced by low level laser therapy (LLLT) irradiation. In this context, the present work was developed in order to investigate if LLLT could reduce dysfunction in inflamed bronchi smooth muscles (BSM) in rats.

STUDY DESIGN/MATERIALS AND METHODS: A controlled ex vivo study was developed where bronchi from Wistar rat were dissected and mounted in an organ bath apparatus with or without a TNF-alpha.

RESULTS: LLLT administered perpendicularly to a point in the middle of the dissected bronchi with a wavelength of 655 nm and a dose of 2.6 J/cm(2), partially decreased BSM hyperreactivity to cholinergic agonist, restored BSM relaxation to isoproterenol and reduced the TNF-alpha mRNA expression. An NF-kappaB antagonist (BMS205820) blocked the LLLT effect on dysfunction in inflamed BSM. CONCLUSION: The results obtained in this work indicate that the LLLT effect on alterations in responsiveness of airway smooth muscles observed in TNF-alpha-induced experimental acute lung inflammation seems to be dependent of NF-kappaB activation.

Inflammation. 2008 Jun;31(3):189-97. Epub 2008 Apr 18.

Low level laser therapy (LLLT) decreases pulmonary microvascular leakage, neutrophil influx and IL-1beta levels in airway and lung from rat subjected to LPS-induced inflammation.

Aimbire F, Ligeiro de Oliveira AP, Albertini R, Corrêa JC, Ladeira de Campos CB, Lyon JP, Silva JA Jr, Costa MS.

Instituto de Pesquisa & Desenvolvimento-IP&D, Universidade do Vale do Paraíba-UNIVAP, Av. Shishima Hifumi, 2911, CEP: 12244-000, São José dos Campos, São Paulo, Brazil. aimbire@univap.br

BACKGROUND AND OBJECTIVE: Low level laser therapy (LLLT) is a known anti-inflammatory therapy. Herein we studied the effect of LLLT on lung permeability and the IL-1beta level in LPS-induced pulmonary inflammation.

STUDY DESIGN/METHODOLOGY: Rats were divided into 12 groups (n = 7 for each group). Lung permeability was measured by quantifying extravasated albumin concentration in lung homogenate, inflammatory cells influx was determined by myeloperoxidase activity, IL-1beta in BAL was determined by ELISA and IL-1beta mRNA expression in trachea was evaluated by RT-PCR. The rats were irradiated on the skin over the upper bronchus at the site of tracheotomy after LPS.

RESULTS: LLLT attenuated lung permeability. In addition, there was reduced neutrophil influx, myeloperoxidase activity and both IL-1beta in BAL and IL-1beta mRNA expression in trachea obtained from animals subjected to LPS-induced inflammation.

CONCLUSION: LLLT reduced the lung permeability by a mechanism in which the IL-1beta seems to have an important role.

Photomed Laser Surg. 2007 Apr;25(2):112-7.

Effect of low-level laser therapy on hemorrhagic lesions induced by immune complex in rat lungs.

Aimbire F, Lopes-Martins RA, Albertini R, Pacheco MT, Castro-Faria-Neto HC, Martins PS, Bjordal JM.

Laboratory of Animal Experimentation, Research and Development Institute (IP&D), Vale do Paraíba University (UNIVAP), São José dos Campos, Brazil.

OBJECTIVE: The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate formation of hemorrhagic lesions induced by immune complex.

BACKGROUND DATA: There is a lack of information on LLLT effects in hemorrhagic injuries of high perfusion organs, and the relative efficacy of LLLT compared to anti-inflammatory drugs.

METHODS: A controlled animal study was undertaken with 49 male Wistar rats randomly divided into seven groups. Bovine serum albumin (BSA) i.v. was injected through the trachea to induce an immune complex lung injury. The study compared the effect of irradiation by a 650-nm Ga-Al-As laser with LLLT doses of 2.6 Joules/cm(2) to celecoxib, dexamethasone, and control groups for hemorrhagic index (HI) and myeloperoxide activity (MPO) at 24 h after injury. RESULTS: The HI for the control group was 4.0 (95% CI, 3.7-4.3). Celecoxib, LLLT, and dexamethasone all induced significantly (p < 0.01) lower HI than control animals at 2.5 (95% CI, 1.9-3.1), 1.8 (95% CI, 1.2-2.4), and 1.5 (95% CI, 0.9-2.1), respectively, for all comparisons to control. Dexamethasone, but not celecoxib, induced a slightly, but significantly lower HI than LLLT (p = 0.04). MPO activity was significantly decreased in groups receiving celecoxib at 0.87 (95% CI, 0.63-1.11), dexamethasone at 0.50 (95% CI, 0.24-0.76), and LLLT at 0.7 (95% CI, 0.44-0.96) when compared to the control group, at 1.6 (95% CI, 1.34-1.96; p < 0.01), but there were no significant differences between any of the active treatments.

CONCLUSION: LLLT at a dose of 2.6 Joules/cm(2) induces a reduction of HI levels and MPO activity in hemorrhagic injury that is not significantly different from celecoxib. Dexamethasone is slightly more effective than LLLT in reducing HI, but not MPO activity.