Laboratory of Experimental Therapeutics LIM20, Department of Medicine, School of Medicine, University of São Paulo, São Paulo, Brazil.
Laboratory of Medical Investigation LIM56, Division of Clinical Dermatology, School of Medicine, University of São Paulo, São Paulo, Brazil.
Front Immunol. 2019 May 16;10:854. doi: 10.3389/fimmu.2019.00854. eCollection 2019.
The benefits of moderate aerobic physical exercise for allergic asthma are well-known, particularly that of the anti-inflammatory effect that occurs by reducing Th2 responses and lung remodeling. However, the mechanisms of this immunoregulation are still under investigation. In this study, we investigated the possible immunoregulatory mechanisms of lung inflammation induced by moderate aerobic exercise in an experimental asthma model. BALB/c mice were distributed into Control, Exercise (EX), OVA, and OEX groups. OVA and OEX groups were sensitized with ovalbumin (OVA) on days 0, 14, 21, 28, and 42 and were challenged with OVA aerosol three times a week from days 21 to 51. The EX and OEX groups underwent moderate aerobic physical exercise from days 21 to 51 (5 d/w, 1 h/d). The mice were euthanized on day 52. We evaluated pulmonary cytokine production, serum immunoglobulin levels, and the inflammatory cell profile in lung and mediastinal lymph nodes. OVA mice showed increased expression of IL-4, IL-6, IL-10, and TGF-β and decreased macrophage type 2 (M2) recruitment. Physical exercise did not affect the increased antibody production of IgG2a, IgG1, or IgE induced by OVA. Of note, physical exercise alone markedly increased production of anti-inflammatory cytokines such as IL-10 and TGF-β. Physical exercise in OVA-mice also increased the recruitment of M2 in the lungs, as well as the influx and activation of regulatory T cells (Tregs) and CD4 and CD8 lymphocytes. In the draining lymph nodes, it was also observed that physical exercise increased the activation of CD4 T cells, regardless of the presence of OVA. Notably, physical exercise decreased common dendritic cells' (cDCs; pro-inflammatory) expression of co-stimulatory molecules such as CD80, CD86, and ICOSL in the draining lymph nodes, as well as increased ICOSL in plasmacytoid dendritic cells (pDCs; anti-inflammatory). Together, these findings show that physical exercise modulates pulmonary allergic inflammation by increasing Treg and M2 recruitment, as well as pDCs activation, which leads to an increase in anti-inflammatory cytokines and a decrease in pro-inflammatory cells and mediators.
中等强度有氧运动对过敏性哮喘的益处是众所周知的,特别是通过减少 Th2 反应和肺重塑来发挥抗炎作用。然而,这种免疫调节的机制仍在研究中。在这项研究中,我们研究了在实验性哮喘模型中中等强度有氧运动引起的肺部炎症的可能免疫调节机制。BALB/c 小鼠分为对照组、运动组(EX)、OVA 组和 OEX 组。OVA 组和 OEX 组在第 0、14、21、28 和 42 天用卵清蛋白(OVA)致敏,从第 21 天到第 51 天每周用 OVA 气溶胶攻击 3 次。EX 和 OEX 组从第 21 天到第 51 天进行中等强度的有氧运动(5 天/周,1 小时/天)。第 52 天处死小鼠。我们评估了肺细胞因子产生、血清免疫球蛋白水平以及肺和纵隔淋巴结中的炎症细胞谱。OVA 组小鼠表现出 IL-4、IL-6、IL-10 和 TGF-β表达增加,M2 型巨噬细胞募集减少。运动没有影响 OVA 诱导的 IgG2a、IgG1 或 IgE 抗体产生的增加。值得注意的是,单独运动明显增加了抗炎细胞因子如 IL-10 和 TGF-β的产生。OVA 组的运动也增加了肺部 M2 的募集,以及调节性 T 细胞(Tregs)和 CD4 和 CD8 淋巴细胞的流入和激活。在引流淋巴结中,也观察到运动增加了 CD4 T 细胞的激活,而不管是否存在 OVA。值得注意的是,运动降低了引流淋巴结中树突状细胞(DCs;促炎)共刺激分子如 CD80、CD86 和 ICOSL 的表达,同时增加了浆细胞样树突状细胞(pDCs;抗炎)中的 ICOSL。总之,这些发现表明,运动通过增加 Treg 和 M2 的募集以及 pDCs 的激活来调节肺部过敏性炎症,从而增加抗炎细胞因子,减少促炎细胞和介质。