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Pulmonary infection byStreptococcus pneumoniae is characterized by a robust alveolar infiltration of neutrophils (polymorphonuclear cells [PMNs]) that can promote systemic spread of the infection if not resolved. We previously showed that 12-lipoxygenase (12-LOX), which is required to generate the PMN chemoattractant hepoxilin A3 (HXA3 ) from arachidonic acid (AA), promotes acute pulmonary inflammation and systemic infection after lung challenge withS. pneumoniae . As phospholipase A2 (PLA2 ) promotes the release of AA, we investigated the role of PLA2 in local and systemic disease duringS. pneumoniae infection. The group IVA cytosolic isoform of PLA2 (cPLA2 α) was activated uponS. pneumoniae infection of cultured lung epithelial cells and was critical for AA release from membrane phospholipids. Pharmacological inhibition of this enzyme blockedS. pneumoniae -induced PMN transepithelial migrationin vitro . Genetic ablation of the cPLA2 isoform cPLA2 α dramatically reduced lung inflammation in mice upon high-dose pulmonary challenge withS. pneumoniae . The cPLA2 α-deficient mice also suffered no bacteremia and survived a pulmonary challenge that was lethal to wild-type mice. Our data suggest that cPLA2 α plays a crucial role in eliciting pulmonary inflammation during pneumococcal infection and is required for lethal systemic infection followingS. pneumoniae lung challenge.

Cytosolic Phospholipase A2α Promotes Pulmonary Inflammation and Systemic Disease during Streptococcus pneumoniae Infection

Cytosolic Phospholipase A₂α Promotes Pulmonary Inflammation and Systemic Disease during Streptococcus pneumoniae Infection