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原标题：氯暴露通过先天淋巴细胞和CD11cint巨噬细胞加重哮喘炎症反应
背景：氯在日常生活中被广泛用于消毒剂。 但是，长期接触氯产品会加剧TH2型过敏性炎症和气道高反应性（AHR）。 气道中的先天淋巴样细胞（ILC）与病毒感染、环境污染和营养过剩有关，这些因素易导致哮喘发作，但长期暴露于氯是否能激活先天免疫细胞尚不清楚。 这项研究的目的是通过使用鼠卵清蛋白（OVA）敏化/挑战模型评估氯吸入对先天免疫（如ILC和巨噬细胞）与哮喘发展相关的影响。
方法：在有或没有慢性低剂量氯暴露的情况下，通过吸入5%次氯酸钠溶液的自然蒸发气体，对六周大的BALB / c雌性小鼠进行OVA致敏和激发。观察支气管肺泡灌洗液（BALF）中气道炎症细胞、肺内ILCs和巨噬细胞的数量。 
结果：与OVA处理的小鼠（OVA组）相比，OVA暴露于氯的小鼠（Cl + OVA组）显示出更强的AHR和嗜酸性炎症。 Cl + OVA组与OVA组相比，TH2细胞，ILC2s和ILC3s的数量增加。 与OVA组相比，Cl + OVA组的CD11cint巨噬细胞也显着增加。 氯膦酸盐清除巨噬细胞导致ILC2s和ILC3s减少，通过过继转移CD11cint巨噬细胞来恢复ILC2s和ILC3数量。
结论：慢性氯气吸入会通过促炎性巨噬细胞移入肺部并刺激ILC2s和ILC3s来加剧哮喘气道中的炎症。


延伸阅读
Allergy                                           
Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages
DOI: 10.1111/all.14017
Abstract:
Background: Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in association with virus infection, pollution, and excess of nutrient, but it is not known whether chronic chlorine exposure can activate innate immune cells. The aim of this study was to evaluate the impact of chlorine inhalation on the innate immunity such as ILCs and macrophages in relation with the development of asthma by using murine ovalbumin (OVA) sensitization/challenge model. 
Methods: Six‐week‐old female BALB/c mice were sensitized and challenged with OVA in the presence and absence of chronic low‐dose chlorine exposure by inhalation of naturally vaporized gas of 5% sodium hypochlorite solution. AHR, airway inflammatory cells, from BALF and the population of ILCs and macrophages in the lung were evaluated.
Results:  The mice exposed to chlorine with OVA (Cl + OVA group) showed enhanced AHR and eosinophilic inflammation compared to OVA‐treated mice (OVA group). The population of TH2 cells, ILC2s, and ILC3s increased in Cl + OVA group compared with OVA group. CD11cint macrophages also remarkably increased in Cl + OVA group compared with OVA group. The deletion of macrophages by clodronate resulted in reduction of ILC2s and ILC3s population which was restored by adoptive transfer of CD11cint macrophages.
Conclusion: Chronic chlorine inhalation contributes to the exacerbation of airway inflammation in asthmatic airway by mobilizing pro‐inflammatory macrophage into the lung as well as stimulating group 2 and 3 ILCs.
First Author:
Ji‐Su Shim 
Correspondence:
Hye Young Kim, Laboratory of mucosal immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐gu, Seoul 03080, Korea.
All Authors:
Ji‐Su Shim, Hyun‐Seung Lee, Da‐Eun Park, Ji Won Lee, Boram Bae, Yuna Chang, Jihyun Kim, Hye Young Kim, Hye‐Ryun Kang
　　创建过敏性疾病的科研、科普知识交流平台，为过敏患者提供专业诊断、治疗、预防的共享平台。