烟草烟雾可通过诱导记忆样3型先天淋巴细胞加重哮喘
2022/07/19
摘要
背景：虽然已知吸烟会加重哮喘，但目前有关吸烟者哮喘的临床研究仍很少。
方法与结果：本文通过比较吸烟和非吸烟哮喘患者的配对痰液和血液样本发现，吸烟与痰中促炎的天然细胞毒性受体非表达3型先天淋巴细胞（ILC3）数量及血液中记忆血液中记忆样CD45RO表达的ILC3显著增加相关。上述ILC3 数量与循环中性粒细胞计数和 M1肺泡巨噬细胞计数呈正相关，而上述变化已知会出现在未控制重症哮喘中，但与过敏性哮喘中的外周血嗜酸性粒细胞计数无关。 ILC体外实验发现，香烟烟雾提取物可诱导 ILC3中记忆标志 CD45RO 表达。香烟烟雾提取物还可损伤气道上皮细胞的屏障功能，并使其产生更多IL-1β，而IL-1β是一种已知ILC3 激活因子。
结论：因此，本研究表明，吸烟可增加局部和循环中活化 ILC3 细胞的数量并参与其活化，进而加重非过敏性炎症和哮喘。
Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells
Ham J, Kim J, Sohn KH, Park IW, Choi BW, Chung DH, Cho SH, Kang HR, Jung JW, Kim HY
Abstract
BACKGROUND：Although cigarette smoking is known to exacerbate asthma, only a few clinical asthma studies have been conducted involving smokers.
METHODS & RESULTS:Here we show, by comparing paired sputum and blood samples from smoking and non-smoking patients with asthma, that smoking associates with significantly higher frequencies of pro-inflammatory, natural-cytotoxicity-receptor-non-expressing type 3 innate lymphoid cells (ILC3) in the sputum and memory-like, CD45RO-expressing ILC3s in the blood. These ILC3 frequencies positively correlate with circulating neutrophil counts and M1 alveolar macrophage frequencies, which are known to increase in uncontrolled severe asthma, yet do not correlate with circulating eosinophil frequencies that characterize allergic asthma. In vitro exposure of ILCs to cigarette smoke extract induces expression of the memory marker CD45RO in ILC3s. Cigarette smoke extract also impairs the barrier function of airway epithelial cells and increases their production of IL-1β, which is a known activating factor for ILC3s.
CONCLUSIONS:Thus, our study suggests that cigarette smoking increases local and circulating frequencies of activated ILC3 cells, plays a role in their activation, thereby aggravating non-allergic inflammation and the severity of asthma.
背景：虽然已知吸烟会加重哮喘，但目前有关吸烟者哮喘的临床研究仍很少。
方法与结果：本文通过比较吸烟和非吸烟哮喘患者的配对痰液和血液样本发现，吸烟与痰中促炎的天然细胞毒性受体非表达3型先天淋巴细胞（ILC3）数量及血液中记忆血液中记忆样CD45RO表达的ILC3显著增加相关。上述ILC3 数量与循环中性粒细胞计数和 M1肺泡巨噬细胞计数呈正相关，而上述变化已知会出现在未控制重症哮喘中，但与过敏性哮喘中的外周血嗜酸性粒细胞计数无关。 ILC体外实验发现，香烟烟雾提取物可诱导 ILC3中记忆标志 CD45RO 表达。香烟烟雾提取物还可损伤气道上皮细胞的屏障功能，并使其产生更多IL-1β，而IL-1β是一种已知ILC3 激活因子。
结论：因此，本研究表明，吸烟可增加局部和循环中活化 ILC3 细胞的数量并参与其活化，进而加重非过敏性炎症和哮喘。
(中日友好医院呼吸与危重症医学科 张婧媛 摘译 林江涛 审校)
(Nat Commun. 2022 Jul 4;13(1):3852. doi: 10.1038/s41467-022-31491-1.)
(Nat Commun. 2022 Jul 4;13(1):3852. doi: 10.1038/s41467-022-31491-1.)
Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells
Ham J, Kim J, Sohn KH, Park IW, Choi BW, Chung DH, Cho SH, Kang HR, Jung JW, Kim HY
Abstract
BACKGROUND：Although cigarette smoking is known to exacerbate asthma, only a few clinical asthma studies have been conducted involving smokers.
METHODS & RESULTS:Here we show, by comparing paired sputum and blood samples from smoking and non-smoking patients with asthma, that smoking associates with significantly higher frequencies of pro-inflammatory, natural-cytotoxicity-receptor-non-expressing type 3 innate lymphoid cells (ILC3) in the sputum and memory-like, CD45RO-expressing ILC3s in the blood. These ILC3 frequencies positively correlate with circulating neutrophil counts and M1 alveolar macrophage frequencies, which are known to increase in uncontrolled severe asthma, yet do not correlate with circulating eosinophil frequencies that characterize allergic asthma. In vitro exposure of ILCs to cigarette smoke extract induces expression of the memory marker CD45RO in ILC3s. Cigarette smoke extract also impairs the barrier function of airway epithelial cells and increases their production of IL-1β, which is a known activating factor for ILC3s.
CONCLUSIONS:Thus, our study suggests that cigarette smoking increases local and circulating frequencies of activated ILC3 cells, plays a role in their activation, thereby aggravating non-allergic inflammation and the severity of asthma.
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