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首页> 外文期刊>Clinical and experimental allergy : >Extracellular vesicles, especially derived from Gram-negative bacteria, in indoor dust induce neutrophilic pulmonary inflammation associated with both Th1 and Th17 cell responses
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Extracellular vesicles, especially derived from Gram-negative bacteria, in indoor dust induce neutrophilic pulmonary inflammation associated with both Th1 and Th17 cell responses

机译：室内尘埃中的细胞外囊泡，尤其是革兰氏阴性菌衍生的细胞外囊泡，可引起与Th1和Th17细胞反应相关的嗜中性肺炎

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摘要

Background: Many bacterial components in indoor dust can evoke inflammatory pulmonary diseases. Bacteria secrete nanometre-sized vesicles into the extracellular milieu, but it remains to be determined whether bacteria-derived extracellular vesicles in indoor dust are pathophysiologically related to inflammatory pulmonary diseases. Objective: To evaluate whether extracellular vesicles (EV) in indoor air are related to the pathogenesis of pulmonary inflammation and/or asthma. Methods: Indoor dust was collected from a bed mattress in an apartment. EV were prepared by sequential ultrafiltration and ultracentrifugation. Innate and adaptive immune responses were evaluated after airway exposure of EV. Results: Repeated intranasal application of indoor-dust-induced neutrophilic pulmonary inflammation accompanied by lung infiltration of both Th1 and Th17 cells. EV 50-200 nm in diameter were present (102.5 μg protein concentration/g dust) in indoor dust. These vesicles were internalized by airway epithelial cells and alveolar macrophages, and this process was blocked by treatment of polymyxin B (an antagonist of lipopolysaccharide, an outer-membrane component of Gram-negative bacteria). Intranasal application of 0.1 or 1 μg of these vesicles for 4 weeks elicited neutrophilic pulmonary inflammation. This phenotype was accompanied by lung infiltration of both Th1 and Th17 cells, which were reversed by treatment of polymyxin B. Serum dust EV-reactive IgG1 levels were significantly higher in atopic children with asthma than in atopic healthy children and those with rhinitis or dermatitis. Conclusion & Clinical Relevance: Indoor dust EV, especially derived from Gram-negative bacteria, is a possible causative agent of neutrophilic airway diseases.
机译：背景：室内灰尘中的许多细菌成分都可以引起炎症性肺部疾病。细菌将纳米大小的囊泡分泌到细胞外环境中，但是室内灰尘中细菌衍生的细胞外囊泡是否在病理生理上与炎性肺部疾病相关，尚待确定。目的：评估室内空气中的细胞外囊泡（EV）是否与肺部炎症和/或哮喘的发病机制有关。方法：从公寓的床褥中收集室内灰尘。通过顺序超滤和超速离心制备EV。 EV气道暴露后评估先天性和适应性免疫反应。结果：反复鼻内应用室内粉尘引起的嗜中性肺炎并伴有Th1和Th17细胞的肺浸润。室内尘埃中存在直径50-200 nm的EV（102.5μg蛋白质浓度/ g尘埃）。这些囊泡被气道上皮细胞和肺泡巨噬细胞内在化，并且该过程被多粘菌素B（脂多糖的一种拮抗剂，革兰氏阴性菌的外膜成分）的治疗所阻断。鼻腔应用0.1或1微克这些囊泡4周引起中性粒细胞肺炎症。这种表型伴有Th1和Th17细胞的肺浸润，通过多粘菌素B的治疗逆转。特应性哮喘儿童的血清尘埃EV反应性IgG1水平显着高于特应性健康儿童和鼻炎或皮炎的儿童。结论与临床意义：室内尘埃电动汽车，尤其是革兰氏阴性细菌衍生的电动汽车，可能是嗜中性气道疾病的致病因素。

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