We reported that Pla2g5-null mice lacking group V secretory phospholipase A 2 (gV-sPLA 2) showed reduced eosinophilic pulmonary inflammation and Th2 cytokine generation when challenged with an extract from house dust mite Dermatophagoides farinae, compared with wild-type (WT) controls. Adoptive transfer studies suggested that gV-sPLA 2 in dendritic cells was necessary for sensitization of Pla2g5-null mice, but was not sufficient to induce the effector phase of pulmonary inflammation. In this study, we demonstrate that gV-sPLA 2 is inducibly expressed in mouse and human macrophages (Mϕ) activated by IL-4 and is required for the acquisition of Mϕ effector functions that facilitate the effector phase of pulmonary inflammation. We demonstrate that gV-sPLA 2 expression in Mϕ is sufficient for the development of pulmonary inflammation, even when inflammation is induced by intrapulmonary administration of IL-4. The concentrations of CCL22/CCL17 and effector T cell recruitment are severely impaired in Pla2g5-null mice. Intratracheal transfers of enriched CD68+ cells isolated from the lungs of D. farinae–challenged WT donor mice induce eosinophilia, chemokine production, and recruitment of T cells into the lungs of Pla2g5-null recipients previously sensitized by WT D. farinae–loaded dendritic cells. Our studies identified a unique function of gV-sPLA 2 in activation of Mϕ and in their capacity to recruit T cells to amplify the effector phase of pulmonary inflammation.