Abstract
Abstract Immune responses have long been associated with pulmonary arterial hypertension. Previous studies in our lab have shown that a prolonged T helper 2 (Th2) response to inhaled antigen induces severe pulmonary arterial remodeling and that this is exacerbated by urban particulate matter (PM) from air pollution. The present study was designed to identify the role of the adaptive immune response (B cells, IL-13, IL-17) in pulmonary hypertension induced by antigen and urban PM. The respirable fraction of airborne PM (PM2.5) was collected in New York City. Th2 primed mice were challenged with soluble antigen (Ovalbumin) combined with urban PM2.5 intranasally. We determined pulmonary arterial remodeling by histology, right heart hypertrophy by ventricular weight measurements and right ventricular systolic pressures recorded in anaesthetized, spontaneously breathing mice. In contrast to wild type, B cell KO mice had no significantly increased right heart weights, or right heart systolic pressures in response to intranasal antigen and urban PM2.5. Reconstitution with anti-antigen antibody restored the development of pulmonary hypertension in these mice. Combined blockade of IL-13 and IL-17 significantly ameliorated pulmonary hypertension induced in wild type mice exposed to antigen and urban PM2.5. Our studies indicate that antigen-specific antibody, IL-13 and IL-17 are necessary for the development of pulmonary hypertension induced by the exposure to antigen and urban PM2.5.
Published Version
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