PM(2.5) impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis

BACKGROUND: 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 (PM(2.5)) is known to significantly contribute to respiratory diseases. PM(2.5)-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM(2.5) exposure on molecular interactions between pneumococcus and macrophages. RESULTS: PM(2.5) exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM(2.5)-exposed pneumococcus-infected mouse model, PM(2.5) subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM(2.5) exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways. CONCLUSIONS: The effect of PM(2.5) exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.