Macrophages expressing group V phospholipase A 2 (Pla2g5) release the Free fatty acid (FFA) linoleic acid (LA), potentiating lung type 2 inflammation. Although Pla2g5 and LA increase in viral infections, their role remains obscure. We generated Pla2g5flox/flox mice, deleted Pla2g5 by using the Cx3Cr1cre transgene, and activated bone marrow-derived macrophages (BM-Macs) with Poly:IC, a synthetic double-stranded RNA that triggers a viral-like immune response, Poly:IC+LA, and known Pla2g5-dependent stimuli (IL-4, LPS+IFNg and IL-33+IL-4+GM-CSF) followed by lipidomic and transcriptomic analysis. In absence of Pla2g5, PolyI: IC-activated BM-Macs had a reduction of major bioactive lipids and critical enzymes producing those bioactive lipids. Additionally, AKT phosphorylation was reduced in Poly:IC stimulated BM-Macs lacking Pla2g5, which was not restored by adding LA to Poly:IC. Furthermore, Pla2g5flox/flox; Cx3cr1cre/+ mice had diminished Poly:IC-induced lung inflammation, including inflammatory macrophage proliferation; adding LA to Poly:IC partially restored lung inflammation. Additionally, mice lacking FFA receptor-1, ( Ffar1)-null mice had reduced Poly: IC-induced lung cell recruitment, not corrected by LA. Thus, Pla2g5 contributes to Poly: IC-induced lung inflammation by regulating inflammatory macrophage proliferation and LA/Ffar1 lung cell recruitment.