■目前,慢性阻塞性肺疾病(COPD)对全球发病率和死亡率有很大影响。CD4+的增加,CD8+细胞表达NF-κB,STAT4、IFN-γ和穿孔素与吸烟习惯有关,吸烟史,气流速率,阻塞和肺气肿。此外,CD4+CD25+Foxp3+调节性T细胞(Tregs)的缺乏可能损害免疫系统的正常功能并导致呼吸道免疫性疾病。另一方面,由Treg细胞和巨噬细胞产生的抗炎细胞因子IL-10,抑制在COPD中表达的几种促炎细胞因子的合成。因此,免疫治疗策略,如光生物调节(PBM),旨在调节细胞因子的水平,COPD的趋化因子和转录因子。因此,这项研究的目的是评估COPD小鼠模型中PBM治疗后肺中CD4STAT4和CD4CD25Foxp3细胞以及CD4IFN-γ和CD4CD25IL-10的产生。
■我们通过气管应用香烟烟雾提取物在C57BL/6小鼠中诱导COPD。应用PMB治疗整个7周,收集支气管肺泡灌洗(BAL)和肺以研究肺中IFN-γ和IL-10的产生。最后一次服用香烟烟雾提取物后(7周结束),24小时后,动物被安乐死。单因素方差分析和NewmanKeuls检验用于统计学分析,显著性水平调整至5%(p<0.05)。
■该结果表明PBM改善了COPD症状,减少炎症细胞的数量(巨噬细胞,中性粒细胞和淋巴细胞),IFN-γ的水平,IL-10增加。我们还观察到胶原蛋白的减少,粘液,支气管收缩指数,肺泡肿大,CD4+,CD8+,CD4+STAT4+,和CD4+IFN-γ+细胞。此外,在治疗组中,我们发现CD4+CD25+Foxp3+和CD4+IL-10+T细胞增加。
■本研究提示PBM治疗可作为COPD的免疫治疗策略。
UNASSIGNED: Currently, Chronic Obstructive Pulmonary Disease (COPD) has a high impact on morbidity and mortality worldwide. The increase of CD4+, CD8+ cells expressing NF-κB, STAT4, IFN-γ and perforin are related to smoking habit, smoking history, airflow rate, obstruction and pulmonary emphysema. Furthermore, a deficiency in CD4+CD25+Foxp3+ regulatory T cells (Tregs) may impair the normal function of the immune system and lead to respiratory immune disease. On the other hand, the anti-inflammatory cytokine IL-10, produced by Treg cells and macrophages, inhibits the synthesis of several pro-inflammatory cytokines that are expressed in COPD. Therefore, immunotherapeutic strategies, such as Photobiomodulation (PBM), aim to regulate the levels of cytokines, chemokines and transcription factors in COPD. Consequently, the objective of this study was to evaluate CD4+STAT4 and CD4+CD25+Foxp3+ cells as well as the production of CD4+IFN- γ and CD4+CD25+IL-10 in the lung after PBM therapy in a COPD mice model.
UNASSIGNED: We induced COPD in C57BL/6 mice through an orotracheal application of cigarette smoke extract. PMB treatment was applied for the entire 7 weeks and Bronchoalveolar lavage (BAL) and lungs were collected to study production of IFN- γ and IL-10 in the lung. After the last administration with cigarette smoke extract (end of 7 weeks), 24 h later, the animals were euthanized. One-way ANOVA followed by NewmanKeuls test were used for statistical analysis with significance levels adjusted to 5% (p < 0.05).
UNASSIGNED: This result showed that PBM improves COPD symptomatology, reducing the number of inflammatory cells (macrophages, neutrophils and lymphocytes), the levels of IFN-γ among others, and increased IL-10. We also observed a decrease of collagen, mucus, bronchoconstriction index, alveolar enlargement, CD4+, CD8+, CD4+STAT4+, and CD4+IFN-γ+ cells. In addition, in the treated group, we found an increase in CD4+CD25+Foxp3+ and CD4+IL-10+ T cells.
UNASSIGNED: This study suggests that PBM treatment could be applied as an immunotherapeutic strategy for COPD.