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dc.contributor.authorChen, L.
dc.contributor.authorPerks, K.
dc.contributor.authorStick, S.
dc.contributor.authorKicic, Anthony
dc.contributor.authorLarcombe, A.
dc.contributor.authorZosky, G.
dc.date.accessioned2018-02-06T06:16:29Z
dc.date.available2018-02-06T06:16:29Z
dc.date.created2018-02-06T05:49:56Z
dc.date.issued2014
dc.date.submitted2018-02-06
dc.identifier.citationChen, L. and Perks, K. and Stick, S. and Kicic, A. and Larcombe, A. and Zosky, G. 2014. House dust mite induced lung inflammation does not alter circulating vitamin D levels. PLoS ONE. 9 (11).
dc.identifier.urihttp://hdl.handle.net/20.500.11937/63322
dc.identifier.doi10.1371/journal.pone.0112589
dc.description.abstract

© 2014 Chen et al. Low circulating levels of 25-hydroxyvitamin D [25(OH)D] are associated with chronic lung diseases such as asthma. However, it is unclear whether vitamin D is involved in disease pathogenesis or is modified by the inflammation associated with the disease process. We hypothesized that allergic inflammation decreases the level of circulating 25(OH)D and tested this using a mice model of house dust mite (HDM) induced allergic airway inflammation. Cellular influx was measured in bronchoalvelar lavage (BAL) fluid, and allergic sensitization and 25(OH)D levels were measured in serum. Exposure to HDM caused a robust inflammatory response in the lung that was enhanced by prior influenza infection. These responses were not associated with any change in circulating levels of 25(OH)D. These data suggest that alterations in circulating 25(OH)D levels induced by Th-2 driven inflammation are unlikely to explain the cross-sectional epidemiological association between vitamin D deficiency and asthma.

dc.publisherPublic Library of Science
dc.titleHouse dust mite induced lung inflammation does not alter circulating vitamin D levels
dc.typeJournal Article
dcterms.dateSubmitted2018-02-06
dcterms.source.volume9
dcterms.source.number11
dcterms.source.issn1932-6203
dcterms.source.titlePLoS ONE
curtin.digitool.pid261492
curtin.identifier.elementsidELEMENTS-190776
curtin.accessStatusOpen access via publisher


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