Pulmonary T cell activation in response to chronic particulate air pollution

摘要

The purpose of this study was to investigate the effects of chronically inhaled particulate matter 2.5 μm (PM 2.5) on inflammatory cell populations in the lung and systemic circulation. A prominent component of air pollution exposure is a systemic inflammatory response that may exaggerate chronic diseases such as atherosclerosis and insulin resistance. T cell response was measured in wild-type C57B/ L6, Foxp3-green fluorescent protein (GFP) "knockin," and chemokine receptor 3 knockout (CXCR3 -/-) mice following 24-28 wk of PM 2.5 or filtered air. Chronic PM 2.5 exposure resulted in increased CXCR3-expressing CD4 + and CD8 + T cells in the lungs, spleen, and blood with elevation in CD11c + macrophages in the lung and oxidized derivatives of 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine in wild-type mice. CXCR3 deficiency decreased T cells in the lung. GFP + regulatory T cells increased with PM 2.5 exposure in the spleen and blood of Foxp3-GFP mice but were present at very low levels in the lung irrespective of PM 2.5 exposure. Mixed lymphocyte cultures using primary, PM 2.5-treated macrophages demonstrated enhanced T cell proliferation. Our experiments indicate that PM 2.5 potentiates a proinflammatory Th1 response involving increased homing of CXCR3 + T effector cells to the lung and modulation of systemic T cell populations.