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Background  Previous work has shown that disruption of the gene for group X secreted phospholipase A 2  (sPLA 2 -X) markedly diminishes airway hyperresponsiveness and remodeling in a mouse asthma model. With the large number of additional sPLA 2 s in the mammalian genome, the involvement of other sPLA 2 s in the asthma model is possible – in particular, the group V sPLA 2  (sPLA 2 -V) that like sPLA 2 -X is highly active at hydrolyzing membranes of mammalian cells.    Methodology and Principal Findings  The allergen-driven asthma phenotype was significantly reduced in sPLA 2 -V-deficient mice but to a lesser extent than observed previously in sPLA 2 -X-deficient mice. The most striking difference observed between the sPLA 2 -V and sPLA 2 -X knockouts was the significant impairment of the primary immune response to the allergen ovalbumin (OVA) in the sPLA 2 -V −/−  mice. The impairment in eicosanoid generation and dendritic cell activation in sPLA2-V −/−  mice diminishes Th2 cytokine responses in the airways.    Conclusions  This paper illustrates the diverse roles of sPLA 2 s in the immunopathogenesis of the asthma phenotype and directs attention to developing specific inhibitors of sPLA 2 -V as a potential new therapy to treat asthma and other allergic disorders.

Key Role of Group V Secreted Phospholipase A2 in Th2 Cytokine and Dendritic Cell-Driven Airway Hyperresponsiveness and Remodeling