Pulmonary T cell activation in response to chronic particulate air pollution

Deiuliis JA, Kampfrath T, Zhong J, Oghumu S, Maiseyeu A, Chen LC, Sun Q, Satoskar AR, Rajagopalan S. Pulmonary T cell activation in response to chronic particulate air pollution. Am J Physiol Lung Cell Mol Physiol 302: L399-L409, 2012. First published December 9, 2011; doi:10.1152/ajplung.00261.2011.-The purpose of this study was to investigate the effects of chronically inhaled particulate matter <2.5 mu m (PM2.5) 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 PM2.5 or filtered air. Chronic PM2.5 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 PM2.5 exposure in the spleen and blood of Foxp3-GFP mice but were present at very low levels in the lung irrespective of PM2.5 exposure. Mixed lymphocyte cultures using primary, PM2.5-treated macrophages demonstrated enhanced T cell proliferation. Our experiments indicate that PM2.5 potentiates a proinflammatory Th1 response involving increased homing of CXCR3(+) T effector cells to the lung and modulation of systemic T cell populations.