• J. Exp. Med. · Apr 2007

    Importance of group X-secreted phospholipase A2 in allergen-induced airway inflammation and remodeling in a mouse asthma model.

    • William R Henderson, Emil Y Chi, James G Bollinger, Ying-tzang Tien, Xin Ye, Luca Castelli, Yuri P Rubtsov, Alan G Singer, Gertrude K S Chiang, Timo Nevalainen, Alexander Y Rudensky, and Michael H Gelb.
    • Center for Allergy and Inflammation, Department of Medicine, University of Washington, Seattle, WA 98109, USA. joangb@u.washington.edu
    • J. Exp. Med. 2007 Apr 16;204(4):865-77.

    AbstractArachidonic acid metabolites, the eicosanoids, are key mediators of allergen-induced airway inflammation and remodeling in asthma. The availability of free arachidonate in cells for subsequent eicosanoid biosynthesis is controlled by phospholipase A(2)s (PLA(2)s), most notably cytosolic PLA(2)-alpha. 10 secreted PLA(2)s (sPLA(2)s) have also been identified, but their function in eicosanoid generation is poorly understood. We investigated the role of group X sPLA(2) (sPLA(2)-X), the sPLA(2) with the highest in vitro cellular phospholipolysis activity, in acute and chronic mouse asthma models in vivo. The lungs of sPLA(2)-X(-/-) mice, compared with those of sPLA(2)-X(+/+) littermates, had significant reduction in ovalbumin-induced infiltration by CD4(+) and CD8(+) T cells and eosinophils, goblet cell metaplasia, smooth muscle cell layer thickening, subepithelial fibrosis, and levels of T helper type 2 cell cytokines and eicosanoids. These data direct attention to sPLA(2)-X as a novel therapeutic target for asthma.

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