Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter
Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter
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DOI：
10.1016/j.jaci.2010.11.039
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发表时间：
2011-05-01
影响因子：
14.2
通讯作者：
Grigg, Jonathan
中科院分区：
文献类型：
--
作者：
Mushtaq, Naseem;Ezzati, Majid;Grigg, Jonathan
背景资料：流行病学研究报告了肺炎与空气动力学直径小于10微米（μ m）的城市颗粒物（PM 10）之间的关联。肺炎链球菌是全球细菌性肺炎的常见原因。迄今为止，城市PM增强肺炎链球菌感染脆弱性的机制尚不清楚。肺炎链球菌与宿主细胞的粘附是感染的先决条件。宿主表达的蛋白质，包括血小板活化因子受体（PAFR），被肺炎链球菌吸收粘附于下呼吸道上皮细胞。目的：确定可吸入的城市PM是否增强肺炎链球菌粘附于呼吸道上皮细胞。A549细胞用来自莱斯特的PM 10培养（英国[UK]）和来自阿克拉（加纳）的空气动力学直径小于2.5 μ m的PM 10和PM（PM 2.5），然后用肺炎链球菌菌株D39感染。还评估了肺炎球菌对人原代支气管上皮细胞的粘附。通过定量培养和共聚焦显微镜测定细菌粘附。氧化应激的作用进行了评估N-乙酰半胱氨酸，和PAFR的作用进行了评估的mRNA转录水平，受体表达，受体blocking.Results：PM10（英国）增加肺炎链球菌粘附到A549气道上皮细胞和人原代支气管上皮细胞。PM10（加纳）和PM2.5（加纳）也增加了粘附性。PM10（UK）培养A549细胞后，PAFR mRNA转录水平和PAFR表达增加。PM10（UK）刺激的粘附A549 cells衰减PAFR阻滞剂和N-乙酰cystein.Conclusion：城市PM增加粘附肺炎链球菌对人气道上皮细胞。PM刺激的粘附由氧化应激和PAFR介导。（《过敏临床免疫学杂志》2011;127：1236-42。）
Background: Epidemiologic studies report an association between pneumonia and urban particulate matter (PM) less than 10 microns (mu m) in aerodynamic diameter (PM10). Streptococcus pneumoniae is a common cause of bacterial pneumonia worldwide. To date, the mechanism whereby urban PM enhances vulnerability to S pneumoniae infection is unclear. Adhesion of S pneumoniae to host cells is a prerequisite for infection. Host-expressed proteins, including the receptor for platelet-activating factor (PAFR), are co-opted by S pneumoniae to adhere to lower airway epithelial cells.Objectives: To define whether inhalable urban PM enhances the adhesion of S pneumoniae to airway epithelial cells.Methods: A549 cells were cultured with PM10 from Leicester (United Kingdom [UK]) and PM10 and PM less than 2.5 mu m in aerodynamic diameter (PM2.5) from Accra (Ghana), then infected with S pneumoniae strain D39. Pneumococcal adhesion to human primary bronchial epithelial cells was also assessed. Bacterial adhesion was determined by quantitative culture and confocal microscopy. The role of oxidative stress was assessed by N-acetyl cysteine, and the role of PAFR was assessed by mRNA transcript level, receptor expression, and receptor blocking.Results: PM10 (UK) increased S pneumoniae adhesion to both A549 airway epithelial cells and human primary bronchial epithelial cells. PM10 (Ghana) and PM2.5 (Ghana) also increased adhesion. Culture of A549 cells by PM10 (UK) increased PAFR mRNA transcript level and PAFR expression. PM10 (UK)-stimulated adhesion to A549 cells was attenuated by a PAFR blocker and N-acetyl cysteine.Conclusion: Urban PM increases adhesion of S pneumoniae to human airway epithelial cells. PM-stimulated adhesion is mediated by oxidative stress and PAFR. (J Allergy Clin Immunol 2011;127:1236-42.)