KU Leuven, Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery, Herestraat 49 box 706, 3000 Leuven, Belgium.
KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology research group, Herestraat 49 box 811, 3000 Leuven, Belgium.
Sci Total Environ. 2022 Oct 15;843:157046. doi: 10.1016/j.scitotenv.2022.157046. Epub 2022 Jun 30.
Exercise-induced bronchoconstriction (EIB) is defined as acute narrowing of the airways during or immediately after exercise. EIB has a high prevalence in elite swimmers probably due to the high ventilation rate and exposure to the chlorine by-products. It is still puzzling which pathophysiological mechanisms drive EIB.
In this study, we evaluated airway hyperreactivity, permeability, integrity and inflammation in a murine swimmers EIB model with and without chlorine exposure.
Mice performed a 3-week swimming protocol in a swimming pool with counter current. Three hours after the last swimming session, airway hyperreactivity to methacholine was assessed. Cytokine levels and cellular differential analysis was performed in BAL fluid. Airway permeability and tight junction expression was measured in serum and lung tissue. T-, B-, dendritic and innate lymphoid cells were determined in lung tissue via flow cytometry.
A significant higher airway resistance (Rn; P < 0.0001) was observed in mice swimming in chlorinated water (mean Rn = 1.26 cmHO.s/ml) compared to mice swimming in tap water (mean Rn = 0.76 cmHO.s/ml) and both inhalation groups in the absence of cellular inflammation. No significant differences were found in lung immune cell populations or in lung tight junction mRNA expression. Experiments in SCID, Rag2γc or Cpa3 mice showed a limited involvement of the innate, adaptive immune system or the mast cells.
Our 3-week swimming murine model mimics intensive swimming in chlorinated water with the presence of airway hyperreactivity in mice swimming in chlorinated water in the absence of airway inflammation and airway epithelial damage.
运动诱发的支气管收缩（EIB）定义为运动期间或运动后立即发生的气道急性变窄。由于高通气率和暴露于氯副产物，精英游泳运动员中 EIB 的患病率很高。是什么导致 EIB 的病理生理机制仍令人费解。
在本研究中，我们评估了暴露于氯和不暴露于氯的游泳运动员 EIB 模型中的气道高反应性、通透性、完整性和炎症。
在逆流游泳池中，对小鼠进行了 3 周的游泳方案。最后一次游泳后 3 小时，评估气道对乙酰甲胆碱的高反应性。BAL 液中进行细胞因子水平和细胞差异分析。血清和肺组织中测量气道通透性和紧密连接表达。通过流式细胞术测定肺组织中的 T、B、树突状和先天淋巴细胞。
与在自来水（平均 Rn = 0.76 cmHO.s/ml）中游泳的小鼠相比，在氯水中游泳的小鼠气道阻力（Rn；P < 0.0001）显著更高（平均 Rn = 1.26 cmHO.s/ml），并且在不存在细胞炎症的情况下，两组吸入组均如此。肺免疫细胞群或肺紧密连接 mRNA 表达没有差异。在 SCID、Rag2γc 或 Cpa3 小鼠中的实验表明，先天、适应性免疫系统或肥大细胞的参与有限。
我们的 3 周游泳小鼠模型模拟了在氯水中进行的强化游泳，在氯水中游泳的小鼠在不存在气道炎症和气道上皮损伤的情况下存在气道高反应性。
