Fig 1.
Treatment with LLLT reduces cell recruitment in the blood (A) but did not alter the number of cells in the bone marrow after FA exposure.
Group of rats was exposed or not to FA inhalation (1%, 90 min/day, 3 days) and treated or not with LLLT (30mW, 1,8 J, 60s/point, total 540s, 1 and 5h post each FA inhalation). Non-manipulated rats were used to obtain basal parameters. The number of cells in the blood (panel A) and in the bone marrow (Panel B) was determined 24 h after the last FA inhalation. Data mean ± SD of 6 animals per group. *P<0.05 in relation to B group; θP<0.05 in relation to FA group.
Fig 2.
Treatment with LLLT reduces neutrophilic lung inflammation after FA exposure.
Group of rats was exposed or not to FA inhalation (1%, 90 min/day, 3 days) and treated or not with LLLT (30mW, 1.8 J, 60s/point, total 540s, 1 and 5h post each FA inhalation). Non-manipulated rats were used to obtain basal parameters. The number of cells in the bronchoalveolar lavage (BAL) (panel A) and myeloperoxidase activity in the lung tissue (MPO) (Panel B) were determined 24 h after the last FA inhalation. Data mean ± SD of 6 animals per group. *P<0.05 in relation to B group; θP<0.05 in relation to FA group.
Fig 3.
Treatment with LLLT reduces lung vascular permeability after FA exposure.
Group of rats was exposed or not to FA inhalation (1%, 90 min/day, 3 days) and treated or not with LLLT (30mW, 1.8 J, 60s/point, total 540s, 1 and 5h post each FA inhalation). Non-manipulated rats were used to obtain basal parameters. The lung vascular permeability in the parenchyma (A), trachea (B) and intrapulmonary bronchi (C) was assessed immediately after the last FA inhalation. Data are mean ± SD of 6 animals per group. *P<0.05 in relation to B group; θP<0.05 in relation to FA group.
Fig 4.
Treatment with LLLT reduces TNF-alpha and IL-6 while increases IL-10 levels in the BAL fluid after FA exposure.
Group of rats was exposed or not to FA inhalation (1%, 90 min/day, 3 days) and treated or not with LLLT (30mW, 1.8 J, 60s/point, total 540s, 1 and 5h post each FA inhalation). Non-manipulated rats were used to obtain basal parameters. The evaluation of inflammatory cytokines TNF-alpha (A) and IL-6 (B) as well as anti-inflammatory IL-10 (C) in the supernatant of BAL fluid were determined 24 h after the last FA exposure. Data are mean ± SD of 6 animals per group. *P<0.05 in relation to B group; θP<0.05 in relation to FA group.
Fig 5.
Treatment with LLLT increases IL-10 gene expression and did not alter IL-6 gene expression in the lung tissue after FA exposure.
Group of rats was exposed or not to FA inhalation (1%, 90 min/day, 3 days) and treated or not with LLLT (30mW, 1.8 J, 60s/point, total 540s, 1 and 5h post each FA inhalation). Non-manipulated rats were used to obtain basal parameters. The evaluation of gene expression of inflammatory cytokine IL-6 (A) and anti-inflammatory IL-10 (B) in the lung were determined 24 h after the last FA exposure. Data are mean ± SD of 6 animals per group. *P<0.05 in relation to B group; θP<0.05 in relation to FA group (Panel B).
Fig 6.
Treatment with LLLT reduces leukocytes infiltration and mast cell degranulation in the lung tissue after FA exposure.
The airway inflammation induced by FA inhalation caused an intense cellular infiltration in the perivascular and peribrochiolar and mast cell activation in the lung parenchyma and pleura (arrows) (Panels C and D), whereas in the basal group, only resident leukocytes were observed and the mast cells were intact (arrowhead) (Panels A and B). Although, after the LLLT treatment, both cellular infiltration and mast cell activation were significantly reduced (Panels E and F).
Table 1.
Effect of treatment with LLLT on leukocytes infiltration and mast cell activation after FA exposure.