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dc.contributor.authorKozul, Courtney D.  Concept link
dc.contributor.authorEly, Kenneth H.  Concept link
dc.contributor.authorEnelow, Richard I.  Concept link
dc.contributor.authorHamilton, Joshua W.  Concept link
dc.date.accessioned2009-09-15T18:56:57Z
dc.date.available2009-09-15T18:56:57Z
dc.date.issued2009-05-20
dc.identifier.citationEnvironmental Health Perspectives 117 (2009): 1441–1447en_US
dc.identifier.urihttps://hdl.handle.net/1912/2991
dc.descriptionThis paper is not subject to U.S. copyright. The definitive version was published in Environmental Health Perspectives 117 (2009): 1441–1447, doi:10.1289/ehp.0900911.en_US
dc.description.abstractArsenic exposure is a significant worldwide environmental health concern. We recently reported that 5-week exposure to environmentally relevant levels (10 and 100 ppb) of As in drinking water significantly altered components of the innate immune response in mouse lung, which we hypothesize is an important contributor to the increased risk of lung disease in exposed human populations. We investigated the effects of As exposure on respiratory influenza A (H1N1) virus infection, a common and potentially fatal disease. In this study, we exposed C57BL/6J mice to 100 ppb As in drinking water for 5 weeks, followed by intranasal inoculation with a sublethal dose of influenza A/PuertoRico/8/34 (H1N1) virus. Multiple end points were assessed postinfection. Arsenic was associated with a number of significant changes in response to influenza, including an increase in morbidity and higher pulmonary influenza virus titers on day 7 postinfection. We also found many alterations in the immune response relative to As-unexposed controls, including a decrease in the number of dendritic cells in the mediastinal lymph nodes early in the course of infection. Our data indicate that chronic As exposure significantly compromises the immune response to infection. Alterations in response to repeated lung infection may also contribute to other chronic illnesses, such as bronchiectasis, which is elevated by As exposure in epidemiology studies.en_US
dc.description.sponsorshipThis work was supported by grant P42 ES007373 from the National Institute of Environmental Health Sciences [J.W.H.; Superfund Basic Research Program (SBRP) Project 2]. C.D.K. was supported by a graduate fellowship from P42 ES007373 (SBRP, Training Core) and by National Institutes of Health predoctoral fellowship T32-DF007301.en_US
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen_US
dc.publisherNational Institute of Environmental Health Sciencesen_US
dc.relation.urihttps://doi.org/10.1289/ehp.0900911
dc.subjectArsenicen_US
dc.subjectDendritic cellsen_US
dc.subjectInfluenzaen_US
dc.subjectInnate immune systemen_US
dc.subjectMouse lungen_US
dc.titleLow-dose arsenic compromises the immune response to influenza A infection in vivoen_US
dc.typeArticleen_US
dc.identifier.doi10.1289/ehp.0900911


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