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dc.contributor.author Gowdy, Kymberly en_US
dc.date.accessioned 2011-06-21T17:30:24Z
dc.date.available 2011-06-21T17:30:24Z
dc.date.issued 2010 en_US
dc.identifier.citation Gowdy,Kymberly M.;Krantz,Quentin T.;King,Charly;Boykin,Elizabeth;Jaspers,Ilona;Linak,William P.;Gilmour,M. Ian. 2010. Role of oxidative stress on diesel-enhanced influenza infection in mice. Particle and Fibre Toxicology 7( ): 34-34. en_US
dc.identifier.issn 1743-8977 en_US
dc.identifier.uri http://hdl.handle.net/10161/4378
dc.description.abstract Numerous studies have shown that air pollutants, including diesel exhaust (DE), reduce host defenses, resulting in decreased resistance to respiratory infections. This study sought to determine if DE exposure could affect the severity of an ongoing influenza infection in mice, and examine if this could be modulated with antioxidants. BALB/c mice were treated by oropharyngeal aspiration with 50 plaque forming units of influenza A/HongKong/8/68 and immediately exposed to air or 0.5 mg/m(3) DE (4 hrs/day, 14 days). Mice were necropsied on days 1, 4, 8 and 14 post-infection and lungs were assessed for virus titers, lung inflammation, immune cytokine expression and pulmonary responsiveness (PR) to inhaled methacholine. Exposure to DE during the course of infection caused an increase in viral titers at days 4 and 8 post-infection, which was associated with increased neutrophils and protein in the BAL, and an early increase in PR. Increased virus load was not caused by decreased interferon levels, since IFN-beta levels were enhanced in these mice. Expression and production of IL-4 was significantly increased on day 1 and 4 p.i. while expression of the Th1 cytokines, IFN-gamma and IL-12p40 was decreased. Treatment with the antioxidant N-acetylcysteine did not affect diesel-enhanced virus titers but blocked the DE-induced changes in cytokine profiles and lung inflammation. We conclude that exposure to DE during an influenza infection polarizes the local immune responses to an IL-4 dominated profile in association with increased viral disease, and some aspects of this effect can be reversed with antioxidants. en_US
dc.language.iso en_US en_US
dc.publisher BIOMED CENTRAL LTD en_US
dc.relation.isversionof doi:10.1186/1743-8977-7-34 en_US
dc.subject respiratory syncytial virus en_US
dc.subject exhaust particle chemicals en_US
dc.subject ambient en_US
dc.subject particulate matter en_US
dc.subject airway epithelial-cells en_US
dc.subject inflammatory responses en_US
dc.subject united-states en_US
dc.subject listeria-monocytogenes en_US
dc.subject engine emissions en_US
dc.subject il-4 en_US
dc.subject production en_US
dc.subject term exposure en_US
dc.subject toxicology en_US
dc.title Role of oxidative stress on diesel-enhanced influenza infection in mice en_US
dc.title.alternative en_US
dc.description.version Version of Record en_US
duke.date.pubdate 2010-11-22 en_US
duke.description.endpage 34 en_US
duke.description.issue en_US
duke.description.startpage 34 en_US
duke.description.volume 7 en_US
dc.relation.journal Particle and Fibre Toxicology en_US

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