Idiopathic pulmonary fibrosis (IPF) is a progressive and chronic inflammatory disease with a poor prognosis and very few available treatment options. Low-level laser therapy (LLLT) has been gaining prominence as a new and effective anti-inflammatory and immunomodulatory agent. Can lung inflammation and the airway remodeling be regulated by LLLT in an experimental model of IPF in C57Bl/6 mice? The present study investigated if laser attenuates cellular migration to the lungs, the airway remodeling as well as pro-fibrotic cytokines secretion from type II pneumocytes and fibroblasts. Mice were irradiated (780 nm and 30 mW) and then euthanized fifteen days after bleomycin-induced lung fibrosis. Lung inflammation and airway remodeling were evaluated through leukocyte counting in bronchoalveolar lavage fluid (BALF) and analysis of collagen in lung, respectively. Inflammatory cells in blood were also measured. For in vitro assays, bleomycin-activated fibroblasts and type II pneumocytes were irradiated with laser. The pro- and anti-inflammatory cytokines level in BALF as well as cells supernatant were measured by ELISA, and the TGFβ in lung was evaluated by flow cytometry. Lung histology was used to analyze collagen fibers around the airways. LLLT reduced both migration of inflammatory cells and deposition of collagen fibers in the lungs. In addition, LLLT downregulated pro-inflammatory cytokines and upregulated the IL-10 secretion from fibroblasts and pneumocytes. Laser therapy greatly reduced total lung TGFβ. Systemically, LLLT also reduced the inflammatory cells counted in blood. There is no statistical difference in inflammatory parameters studied between mice of the basal group and the laser-treated mice. Data obtained indicate that laser effectively attenuates the lung inflammation, and the airway remodeling in experimental pulmonary fibrosis is driven to restore the balance between the pro- and anti-inflammatory cytokines in lung and inhibit the pro-fibrotic cytokines secretion from fibroblasts.

中文翻译：

---

在特发性肺纤维化的小鼠模型中，低水平激光疗法可减轻肺部炎症和气道重塑：与肺结构细胞分泌的细胞因子有关。

特发性肺纤维化（IPF）是一种进行性和慢性炎性疾病，预后较差，可用的治疗选择很少。低水平激光疗法（LLLT）作为一种新型且有效的抗炎和免疫调节剂而日益受到关注。在C57Bl / 6小鼠IPF实验模型中，LLLT可以调节肺部炎症和气道重塑吗？本研究调查了激光是否能减弱细胞向肺的迁移，气道重塑以及II型肺细胞和成纤维细胞分泌的促纤维化细胞因子。博来霉素诱导的肺纤维化后十五天，对小鼠进行辐射（780 nm和30 mW），然后安乐死。通过支气管肺泡灌洗液（BALF）中的白细胞计数以及肺中胶原蛋白的分析来评估肺部炎症和气道重塑 分别。还测量了血液中的炎性细胞。为了进行体外测定，用激光照射博来霉素活化的成纤维细胞和II型肺细胞。通过ELISA测定BALF中的促炎和抗炎细胞因子水平以及细胞上清液，并且通过流式细胞术评估肺中的TGFβ。肺组织学用于分析气道周围的胶原纤维。LLLT减少了炎症细胞的迁移和胶原纤维在肺中的沉积。此外，LLLT下调了促炎细胞因子，并上调了成纤维细胞和肺细胞的IL-10分泌。激光治疗大大降低了总肺TGFβ。全身而言，LLLT还减少了血液中的炎症细胞计数。在基础组的小鼠和经激光治疗的小鼠之间研究的炎性参数没有统计学差异。所获得的数据表明，激光有效地减轻了肺部炎症，并且驱动了实验性肺纤维化中的气道重塑，以恢复肺部促炎和抗炎细胞因子之间的平衡，并抑制了成纤维细胞促纤维化细胞因子的分泌。