Diesel exposure suppresses natural killer cell function and resolution of eosinophil inflammation: a randomized controll
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Diesel exposure suppresses natural killer cell function and resolution of eosinophil inflammation: a randomized controlled trial of exposure in allergic rhinitics Erica A. Pawlak1, Terry L. Noah1,2, Haibo Zhou3, Claire Chehrazi4, Carole Robinette1, David Diaz-Sanchez5, Loretta Müller6 and Ilona Jaspers1,2*
Abstract Exposure to diesel exhaust (DE) is known to exacerbate allergic inflammation, including virus-induced eosinophil activation in laboratory animals. We have previously shown that in human volunteers with allergic rhinitis a shortterm exposure to DE prior to infection with the live attenuated influenza virus (LAIV) increases markers of allergic inflammation in the nasal mucosa. Specifically, levels of eosinophilic cationic protein (ECP) were significantly enhanced in individuals exposed to DE prior to inoculation with LAIV and this effect was maintained for at least seven days. However, this previous study was limited in its scope of nasal immune endpoints and did not explore potential mechanisms mediating the prolonged exacerbation of allergic inflammation caused by exposure to DE prior to inoculation with LAIV. In this follow-up study, the methods were modified to expand experimental endpoints and explore the potential role of NK cells. The data presented here suggest DE prolongs viral-induced eosinophil activation, which was accompanied by decreased markers of NK cell recruitment and activation. Separate in vitro studies showed that exposure to DE particles decreases the ability of NK cells to kill eosinophils. Taken together, these follow-up studies suggest that DE-induced exacerbation of allergic inflammation in the context of viral infections may be mediated by decreased activity of NK cells and their ability to clear eosinophils. Keywords: Natural killer cell, Diesel exhaust, Eosinophil, Resolution of inflammation
Background Studies in experimental animal models and controlled human exposures suggest that exposure to diesel exhaust (DE) or DE particles may act to heighten allergic respiratory inflammation and immune responses, especially in the context of viral infections [1, 2]. We have previously demonstrated that in mice sensitized to ovalbumin, exposure to DE particles prior to infection with influenza virus significantly enhances allergic inflammation, as marked by influx of eosinophils [3]. Similarly, published data from our group found that short-term * Correspondence: [email protected] 1 Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina at Chapel Hill, 104 Mason Farm Rd, Campus Box 7310, Chapel Hill, NC 27599-7310, USA 2 Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Full list of author information is available at the end of the article
exposure of human volunteers to DE (100 μg/m3 for 2 h) significantly increases live attenuated influenza virus (LAIV)-induced eosinophilic cationic protein (ECP) levels and virus quantity in nasal secretions of allergic rhinitic adult volun
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