原標(biāo)題：氯暴露通過先天淋巴細(xì)胞和CD11cint巨噬細(xì)胞加重哮喘炎癥反應(yīng)
背景：氯在日常生活中被廣泛用于消毒劑。 但是，長(zhǎng)期接觸氯產(chǎn)品會(huì)加劇TH2型過敏性炎癥和氣道高反應(yīng)性（AHR）。 氣道中的先天淋巴樣細(xì)胞（ILC）與病毒感染、環(huán)境污染和營(yíng)養(yǎng)過剩有關(guān)，這些因素易導(dǎo)致哮喘發(fā)作，但長(zhǎng)期暴露于氯是否能激活先天免疫細(xì)胞尚不清楚。 這項(xiàng)研究的目的是通過使用鼠卵清蛋白（OVA）敏化/挑戰(zhàn)模型評(píng)估氯吸入對(duì)先天免疫（如ILC和巨噬細(xì)胞）與哮喘發(fā)展相關(guān)的影響。
方法：在有或沒有慢性低劑量氯暴露的情況下，通過吸入5%次氯酸鈉溶液的自然蒸發(fā)氣體，對(duì)六周大的BALB / c雌性小鼠進(jìn)行OVA致敏和激發(fā)。觀察支氣管肺泡灌洗液（BALF）中氣道炎癥細(xì)胞、肺內(nèi)ILCs和巨噬細(xì)胞的數(shù)量。 
結(jié)果：與OVA處理的小鼠（OVA組）相比，OVA暴露于氯的小鼠（Cl + OVA組）顯示出更強(qiáng)的AHR和嗜酸性炎癥。 Cl + OVA組與OVA組相比，TH2細(xì)胞，ILC2s和ILC3s的數(shù)量增加。 與OVA組相比，Cl + OVA組的CD11cint巨噬細(xì)胞也顯著增加。 氯膦酸鹽清除巨噬細(xì)胞導(dǎo)致ILC2s和ILC3s減少，通過過繼轉(zhuǎn)移CD11cint巨噬細(xì)胞來恢復(fù)ILC2s和ILC3數(shù)量。
結(jié)論：慢性氯氣吸入會(huì)通過促炎性巨噬細(xì)胞移入肺部并刺激ILC2s和ILC3s來加劇哮喘氣道中的炎癥。


延伸閱讀
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
　　創(chuàng)建過敏性疾病的科研、科普知識(shí)交流平臺(tái)，為過敏患者提供專業(yè)診斷、治療、預(yù)防的共享平臺(tái)。