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Role of multidrug resistance-associated protein 1 in the pathogenesis of allergic airway inflammation.

Authors: Yoshioka, M  Sagara, H  Takahashi, F  Harada, N  Nishio, K  Mori, A  Ushio, H  Shimizu, K  Okada, T  Ota, M  Ito, YM  Nagashima, O  Atsuta, R  Suzuki, T  Fukuda, T  Fukuchi, Y  Takahashi, K 
Citation: Yoshioka M, etal., Am J Physiol Lung Cell Mol Physiol. 2009 Jan;296(1):L30-6. Epub 2008 Oct 17.
Pubmed: (View Article at PubMed) PMID:18931056
DOI: Full-text: DOI:10.1152/ajplung.00026.2008

Multidrug resistance-associated protein 1 (MRP1) is a cysteinyl leukotriene (CysLT) export pump expressed on mast cells. CysLTs are crucial mediators in allergic airway disease. However, biological significance of MRP1 in allergic airway inflammation has not yet been elucidated. In this study, we sensitized wild-type control mice (mrp1(+/+)) and MRP1-deficient mice (mrp1(-/-)) to ovalbumin (OVA) and challenged them with OVA by aerosol. Airway inflammation and goblet cell hyperplasia after OVA exposure were reduced in mrp1(-/-) mice compared with mrp1(+/+) mice. Furthermore, CysLT levels in bronchoalveolar lavage fluid (BALF) from OVA-exposed mrp1(-/-) mice were significantly lower than those from OVA-exposed mrp1(+/+) mice. Levels of OVA-specific IgE, IL-4, and IL-13 in BALF were also decreased in OVA-exposed mrp1(-/-) mice. IgE-mediated release of CysLTs from murine bone marrow-derived mast cells was markedly impaired by MRP1 deficiency. Our results indicate that MRP1 plays an important role in the development of allergic airway inflammation through regulation of IgE-mediated CysLT export from mast cells.


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CRRD Object Information
CRRD ID: 5128825
Created: 2011-03-18
Species: All species
Last Modified: 2011-03-18
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.