Biomass smoke exposure is associated with a heightened risk of development of respiratory diseases that include chronic obstructive pulmonary disease (COPD). The aim of this study was to increase our understanding of how biomass smoke could contribute to an increased susceptibility to respiratory infection. We investigated the effects of cow dung and wood smoke exposure on human bronchial epithelial cells with respect to adherence of a major respiratory bacterial pathogen in COPD, nontypeable Haemophilus influenzae (NTHi), using immunofluorescence microscopy. In addition, expression of a known receptor of NTHi, platelet-activating factor receptor (PAFR), and two pro-inflammatory cytokines, interleukin 6 (IL-6) and interleukin-8 (IL-8), were determined using quantitative polymerase chain reaction. We observed a dose-dependent increase in NTHi adhesion to human bronchial epithelial cells following exposure to cow dung but not wood smoke extracts. Pre-treatment with PAFR antagonists, WEB-2086 and its analogue, C17, decreased adherence by NTHi to airway epithelial cells exposed to cow dung smoke. Both cow dung and wood smoke-induced expression of PAFR, as well as of IL-6 and IL-8, which was inhibited by WEB-2086 and C17. In conclusion, biomass smoke from combustion of cow dung and wood-induced expression of PAFR and airway inflammatory markers in human bronchial epithelial cells. Cow dung exposure, but not wood smoke exposure, mediated a measurable increase in NTHi adhesion to airway epithelial cells that was inhibited by PAFR antagonists. This work highlights the potential of PAFR as a therapeutic target for reducing the impact of hazardous biomass smoke exposure on respiratory health.

暴露于生物量烟雾中与罹患包括慢性阻塞性肺疾病（COPD）在内的呼吸系统疾病的风险增加有关。这项研究的目的是增进我们对生物质烟雾如何导致呼吸道感染易感性的了解。我们调查了牛粪和木烟暴露对人支气管上皮细胞的影响，并与COPD，非分型流感嗜血杆菌中主要呼吸道细菌病原体的粘附有关（NTHi），使用免疫荧光显微镜检查。此外，使用定量聚合酶链测定了已知的NTHi受体，血小板活化因子受体（PAFR）和两种促炎细胞因子白介素6（IL-6）和白介素8（IL-8）的表达。反应。我们观察到暴露于牛粪后而不是木烟提取物后，NTHi对人支气管上皮细胞粘附的剂量依赖性增加。用PAFR拮抗剂WEB-2086及其类似物C17进行预处理，可减少NTHi对暴露于牛粪烟雾的气道上皮细胞的粘附。牛粪和木烟都诱导了PAFR以及IL-6和IL-8的表达，该表达被WEB-2086和C17抑制。结论，牛粪燃烧产生的生物质烟雾以及木材诱导的人支气管上皮细胞中PAFR和气道炎症标记物的表达。牛粪暴露而不是木烟暴露介导了NTHi对气道上皮细胞粘附的可测量增加，这被PAFR拮抗剂抑制。这项工作强调了PAFR作为减少有害生物质烟雾暴露对呼吸系统健康的影响的治疗目标的潜力。