Pneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5) is known to significantly contribute to respiratory diseases. PM2.5-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM2.5 exposure on molecular interactions between pneumococcus and macrophages. PM2.5 exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM2.5-exposed pneumococcus-infected mouse model, PM2.5 subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM2.5 exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways. The effect of PM2.5 exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.

中文翻译：

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PM2.5损害巨噬细胞功能，加剧肺炎球菌诱发的肺部发病机制。

肺炎球菌是导致威胁生命的感染的最常见的人类呼吸道病原体之一。已知空气动力学直径≤2.5μm（PM2.5）的环境细颗粒物（PM）会严重导致呼吸系统疾病。PM2.5诱导的气道炎症可能会降低针对细菌感染的先天免疫防御能力。但是，目前关于PM2.5暴露对肺炎球菌和巨噬细胞之间分子相互作用的影响的信息有限。对肺炎球菌感染，PM2.5暴露会阻碍巨噬细胞功能，包括吞噬作用和促炎细胞因子的产生。在暴露于PM2.5的肺炎球菌感染的小鼠模型中，PM2.5破坏了肺部免疫反应并引起白细胞浸润。此外，PM2。5暴露通过抑制PI3K / Akt和MAPK途径抑制了CXCL10及其受体CXCR3的水平。PM2.5暴露对巨噬细胞活性的影响增强了肺炎球菌感染性并加重了肺部发病机理。