氯暴露通过固有淋巴细胞和CD11c中间型巨噬细胞加重哮喘炎症
2020/02/11
摘要
背景：氯在日常生活中被广泛用作消毒剂。然而，长期接触氯气产品会加重TH2型过敏性炎症和气道高反应性(AHR)。气道内的固有淋巴细胞(ILCs)是哮喘发病的重要因素，其与病毒感染、污染和营养过剩有关，但长期氯暴露是否能激活固有免疫细胞尚不清楚。本研究的目的是利用小鼠卵清蛋白(OVA)敏化/挑战模型，评估氯吸入对固有淋巴细胞和巨噬细胞等固有免疫系统的影响与哮喘发生的关系。
方法：六周大的雌性BALB/c小鼠通过吸入有或没有慢性低剂量氯（5%次氯酸钠溶液）的卵清蛋白OVA自然汽化的气体致敏。评估小鼠的气道高反应性、BALF气道炎症细胞、肺内ILCs和巨噬细胞的数量。
结果：与经卵清蛋白（OVA）处理的小鼠(OVA组)相比，经卵清蛋白处理且暴露于氯的小鼠(Cl+OVA组)气道高反应性和嗜酸性炎症反应增强。与OVA组相比，Cl+OVA组的TH2细胞、ILC2s和ILC3s的数量增加。与OVA组相比，Cl+OVA组CD11c中间型巨噬细胞明显增多。氯膦酸盐对巨噬细胞的清除导致ILC2s和ILC3s的减少，通过过继转移CD11c中间型巨噬细胞恢复ILC2s和ILC3s的数量。
结论：长期氯吸入可通过动员促炎巨噬细胞进入肺，刺激第2组和第3组ILCs，加重哮喘气道炎症。
Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages.
Shim JS et al. Allergy. 2019 Aug 11.
Abstract
BACKGROUND:Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH 2 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 is 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 TH 2 cells, ILC2s and ILC3s increased in Cl+OVA group compared to OVA group. CD11cint macrophages also remarkably increased in Cl+OVA group compared to 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.
CONCLUSIONS: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.
背景：氯在日常生活中被广泛用作消毒剂。然而，长期接触氯气产品会加重TH2型过敏性炎症和气道高反应性(AHR)。气道内的固有淋巴细胞(ILCs)是哮喘发病的重要因素，其与病毒感染、污染和营养过剩有关，但长期氯暴露是否能激活固有免疫细胞尚不清楚。本研究的目的是利用小鼠卵清蛋白(OVA)敏化/挑战模型，评估氯吸入对固有淋巴细胞和巨噬细胞等固有免疫系统的影响与哮喘发生的关系。
方法：六周大的雌性BALB/c小鼠通过吸入有或没有慢性低剂量氯（5%次氯酸钠溶液）的卵清蛋白OVA自然汽化的气体致敏。评估小鼠的气道高反应性、BALF气道炎症细胞、肺内ILCs和巨噬细胞的数量。
结果：与经卵清蛋白（OVA）处理的小鼠(OVA组)相比，经卵清蛋白处理且暴露于氯的小鼠(Cl+OVA组)气道高反应性和嗜酸性炎症反应增强。与OVA组相比，Cl+OVA组的TH2细胞、ILC2s和ILC3s的数量增加。与OVA组相比，Cl+OVA组CD11c中间型巨噬细胞明显增多。氯膦酸盐对巨噬细胞的清除导致ILC2s和ILC3s的减少，通过过继转移CD11c中间型巨噬细胞恢复ILC2s和ILC3s的数量。
结论：长期氯吸入可通过动员促炎巨噬细胞进入肺，刺激第2组和第3组ILCs，加重哮喘气道炎症。
（中国医科大学附属第一医院 李文扬 摘译 杨冬 审校）
（Shim JS et al. Allergy. 2019 Aug 11.）
（Shim JS et al. Allergy. 2019 Aug 11.）
Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages.
Shim JS et al. Allergy. 2019 Aug 11.
Abstract
BACKGROUND:Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH 2 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 is 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 TH 2 cells, ILC2s and ILC3s increased in Cl+OVA group compared to OVA group. CD11cint macrophages also remarkably increased in Cl+OVA group compared to 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.
CONCLUSIONS: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.
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了解哮喘中的夏科-雷登结晶
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人气道上皮细胞外囊泡miRNA特征随哮喘发展改变
