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Role of oxidative stress on diesel-enhanced influenza infection in mice

dc.contributor.author Gowdy, Kymberly M
dc.contributor.author Krantz, Quentin T
dc.contributor.author King, Charly
dc.contributor.author Boykin, Elizabeth
dc.contributor.author Jaspers, Ilona
dc.contributor.author Linak, William P
dc.contributor.author Gilmour, M Ian
dc.date.accessioned 2011-06-21T17:30:24Z
dc.date.available 2011-06-21T17:30:24Z
dc.date.issued 2010
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.
dc.identifier.issn 1743-8977
dc.identifier.uri https://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.
dc.language.iso en_US
dc.publisher Springer Science and Business Media LLC
dc.relation.isversionof 10.1186/1743-8977-7-34
dc.subject respiratory syncytial virus
dc.subject exhaust particle chemicals
dc.subject ambient
dc.subject particulate matter
dc.subject airway epithelial-cells
dc.subject inflammatory responses
dc.subject united-states
dc.subject listeria-monocytogenes
dc.subject engine emissions
dc.subject il-4
dc.subject production
dc.subject term exposure
dc.subject toxicology
dc.title Role of oxidative stress on diesel-enhanced influenza infection in mice
dc.title.alternative
dc.type Other article
dc.description.version Version of Record
duke.date.pubdate 2010-11-22
duke.description.issue
duke.description.volume 7
dc.relation.journal Particle and Fibre Toxicology
pubs.begin-page 34


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