Navegando por Palavras-chave "Acute lung inflammation"

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    Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome
    (Springer, 2011-05-01) Lima, Flavia Mafra de; Moreira, Leonardo M.; Villaverde, A. B.; Albertini, Regiane; Castro-Faria-Neto, Hugo C.; Aimbire, Flavio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Res & Dev Inst IP&D; Dept Biosyst Engn; Unicastelo; Ctr Univ Nove Julho Uninove; Fiocruz MS
    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.
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    Suppressive effect of low-level laser therapy on tracheal hyperresponsiveness and lung inflammation in rat subjected to intestinal ischemia and reperfusion
    (Springer, 2013-02-01) Lima, Flavia Mafra de; Vitoretti, Luana; Coelho, Fernando; Albertini, Regiane; Breithaupt-Faloppa, Ana Cristina; Lima, Wothan Tavares de; Aimbire, Flavio [UNIFESP]; Univ Nove Julho; Universidade de São Paulo (USP); Inst Quim; Universidade Federal de São Paulo (UNIFESP)
    Intestinal ischemia and reperfusion (i-I/R) is an insult associated with acute respiratory distress syndrome (ARDS). It is not known if pro- and anti-inflammatory mediators in ARDS induced by i-I/R can be controlled by low-level laser therapy (LLLT). This study was designed to evaluate the effect of LLLT on tracheal cholinergic reactivity dysfunction and the release of inflammatory mediators from the lung after i-I/R. Anesthetized rats were subjected to superior mesenteric artery occlusion (45 min) and killed after clamp release and preestablished periods of intestinal reperfusion (30 min, 2 or 4 h). the LLLT (660 nm, 7.5 J/cm(2)) was carried out by irradiating the rats on the skin over the right upper bronchus for 15 and 30 min after initiating reperfusion and then euthanizing them 30 min, 2, or 4 h later. Lung edema was measured by the Evans blue extravasation technique, and pulmonary neutrophils were determined by myeloperoxidase (MPO) activity. Pulmonary tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1), and isoform of NO synthase (iNOS) mRNA expression were analyzed by real-time PCR. TNF-alpha, IL-10, and iNOS proteins in the lung were measured by the enzyme-linked immunoassay technique. LLLT (660 nm, 7.5 J/cm(2)) restored the tracheal hyperresponsiveness and hyporesponsiveness in all the periods after intestinal reperfusion. Although LLLT reduced edema and MPO activity, it did not do so in all the postreperfusion periods. It was also observed with the ICAM-1 expression. in addition to reducing both TNF-alpha and iNOS, LLLT increased IL-10 in the lungs of animals subjected to i-I/R. the results indicate that LLLT can control the lung's inflammatory response and the airway reactivity dysfunction by simultaneously reducing both TNF-alpha and iNOS.