Underground railway particulate matter and susceptibility to pneumococcal infection.
Underground railway particulate matter and susceptibility to pneumococcal infection.
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DOI：
10.1016/j.ebiom.2022.104063
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发表时间：
2022-06
期刊：
影响因子：
11.1
通讯作者：
Grigg, Jonathan
中科院分区：
文献类型：
--
作者：
Miyashita, Lisa;Shears, Rebecca;Foley, Gary;Semple, Sean;Kadioglu, Aras;Grigg, Jonathan
地下铁路上小于10微米的颗粒物（PM10）浓度高于城市道路附近。肺炎相关的PM10通过增加血小板活化因子受体（PAFR）的表达来增加肺炎球菌感染，PAFR是肺炎球菌选择粘附于细胞的受体。到目前为止，还不清楚地铁PM10是否会增加肺炎球菌感染。本研究旨在确定伦敦地铁（LU）PM10对以下方面的影响：i）肺炎球菌粘附于气道细胞，ii）对肺炎球菌疾病的易感性。使用来自贝克街站Bakerloo（B-PM 10）和Jubilee（J-PM 10）线平台的20 µg/mL PM 10培养A549细胞和人原代气道上皮细胞。PAFR表达通过流式细胞术评估，肺炎球菌粘附通过菌落形成单位（CFU）计数评估。在车站入口附近的一条主要道路旁收集了与空气有关的PM10。PAFR阻断剂CV 3988和抗氧化剂N-乙酰半胱氨酸分别用于评估PAFR介导的肺炎球菌粘附和氧化应激的作用。在暴露于3×80 μg剂量的鼻内LU-PM10后，进行小鼠的肺炎球菌感染。在A549细胞、人原代鼻细胞和人原代支气管上皮细胞中，B-PM 10和J-PM 10增加PAFR表达和肺炎球菌粘附。刺激的粘附被CV 3988和N-乙酰半胱氨酸废除。与B-PM10相比，与B-PM10相关的PM10刺激增加粘附。B-PM 10和J-PM 10增加小鼠肺和血液CFU和死亡率。用CV 3988处理暴露于B-PM10的小鼠降低了血液CFU。LU-PM10增加小鼠中肺炎球菌对气道细胞的粘附和对侵袭性疾病的易感性。圣巴塞洛缪医学院医院信托基金和英国医学研究理事会计划赠款（MR/P011284/1）。
Concentrations of particulate matter less than 10 microns (PM10) on underground railways are higher than those near urban roads. Traffic-related PM10 increases pneumococcal infection via increasing the expression of platelet-activating factor receptor (PAFR), a receptor co-opted by pneumococci to adhere to cells. To date, it is unknown whether underground railway PM10 increases pneumococcal infection. This study sought to determine the effect of London Underground (LU) PM10 on; i) pneumococcal adhesion to airway cells, and ii) susceptibility to pneumococcal disease. A549 cells and human primary airway epithelial cells were cultured with 20 µg/mL PM10 from the Bakerloo (B-PM10) and Jubilee (J-PM10) line platforms of Baker Street station. PAFR expression was assessed by flow cytometry, and pneumococcal adhesion by colony forming unit (CFU) counts. Traffic-related PM10 was collected next to a main road near the station's entrance. The PAFR blocker CV3988 and the antioxidant N-acetyl cysteine were used to assess the role of PAFR-mediated pneumococcal adhesion and oxidative stress respectively. Pneumococcal infection of mice was done after exposure to 3×80 μg doses of intranasal LU-PM10. In A549 cells, human primary nasal cells, and human primary bronchial epithelial cells, B-PM10 and J-PM10 increased PAFR expression and pneumococcal adhesion. Stimulated adhesion was abrogated by CV3988 and N-acetyl cysteine. Traffic-related PM10 stimulated increased adhesion compared with B-PM10. B-PM10 and J-PM10 increased lung and blood CFU and mortality in mice. Treatment of B-PM10-exposed mice with CV3988 reduced blood CFU. LU-PM10 increases pneumococcal adhesion to airway cells and susceptibility to invasive disease in mice. The Medical College of Saint Bartholomew's Hospital Trust, and the UK Medical Research Council Programme Grant (MR/P011284/1).
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