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Key Role of Group V Secreted Phospholipase A2 in Th2 Cytokine and Dendritic Cell-Driven Airway Hyperresponsiveness and Remodeling.
- Source :
- PLoS ONE; Feb2013, Vol. 8 Issue 2, p1-16, 16p
- Publication Year :
- 2013
-
Abstract
- Background: Previous work has shown that disruption of the gene for group X secreted phospholipase A<subscript>2</subscript> (sPLA<subscript>2</subscript>-X) markedly diminishes airway hyperresponsiveness and remodeling in a mouse asthma model. With the large number of additional sPLA<subscript>2</subscript>s in the mammalian genome, the involvement of other sPLA<subscript>2</subscript>s in the asthma model is possible – in particular, the group V sPLA<subscript>2</subscript> (sPLA<subscript>2</subscript>-V) that like sPLA<subscript>2</subscript>-X is highly active at hydrolyzing membranes of mammalian cells. Methodology and Principal Findings: The allergen-driven asthma phenotype was significantly reduced in sPLA<subscript>2</subscript>-V-deficient mice but to a lesser extent than observed previously in sPLA<subscript>2</subscript>-X-deficient mice. The most striking difference observed between the sPLA<subscript>2</subscript>-V and sPLA<subscript>2</subscript>-X knockouts was the significant impairment of the primary immune response to the allergen ovalbumin (OVA) in the sPLA<subscript>2</subscript>-V<superscript>−/−</superscript> mice. The impairment in eicosanoid generation and dendritic cell activation in sPLA2-V<superscript>−/−</superscript> mice diminishes Th2 cytokine responses in the airways. Conclusions: This paper illustrates the diverse roles of sPLA<subscript>2</subscript>s in the immunopathogenesis of the asthma phenotype and directs attention to developing specific inhibitors of sPLA<subscript>2</subscript>-V as a potential new therapy to treat asthma and other allergic disorders. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19326203
- Volume :
- 8
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- PLoS ONE
- Publication Type :
- Academic Journal
- Accession number :
- 87624354
- Full Text :
- https://doi.org/10.1371/journal.pone.0056172