Infrared low-level diode laser on inflammatory process modulation in mice: pro- and anti-inflammatory cytokines

To evaluate the modulation of proinflammatory (interleukin-6, IL-6; tumor necrosis factor-α, TNF-α; and interferon-γ, IFN-γ) and anti-inflammatory cytokines (transforming growth factor-β1, TGF-β1) in the inflammation processes in vivo with low-level laser action, 50 isogenic mice were randomly distributed into three groups: control (no surgical procedure, n = 10), sham (surgical procedure with three standard cutaneous incisions, followed by an abdominal muscle incision and suture, n = 20), and laser (same procedure followed by laser exposure, n = 20). The sham group was divided into three subgroups: sham I (euthanasia and evaluation, 36 h after surgical procedure), sham II (euthanasia and evaluation, 60 h after surgical procedure), and sham III (euthanasia and evaluation, 84 h after surgical procedure). The laser group was also divided in three subgroups: laser I (a single laser session, 12 h after surgery), laser II (two laser sessions, 12 and 36 h after surgery), and laser III (three laser sessions, 12, 36, and 60 h after surgery). All animals in the laser groups received three points per session of continuous infrared laser (wavelength of 780 nm, power of 20 mW, fluency of 10 J/cm 2 , exposure time of 20 s per point, and energy of 0.4 J). After euthanasia, spleen mononuclear cells were isolated and cultured for 48 h. Concentrations of IL-6, TNF-α, IFN-γ, and TGF-β1 were obtained by enzyme-linked immunosorbent assay method. There was a significant difference between the IL-6 and TNF-α concentrations in the 60-and 84-h evaluations when the laser and sham groups were compared to the control group ( p 0.05). The IFN-γ concentration analysis showed a significant difference only in sham II when compared to the control group ( p 0.05). The low-level laser application decreased the TNF-α and IFN-γ release in vivo of spleen mononuclear cells in mice, especially after two exposure sessions. However, there was no modulation of the IL-6 and TGF-β1 release.