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Lipophosphoglycan (LPG) is a key virulence factor expressed on the surfaces of  Leishmania  promastigotes. Although LPG is known to activate macrophages, the underlying mechanisms resulting in the production of prostaglandin E 2  (PGE 2 ) via signaling pathways remain unknown. Here, the inflammatory response arising from stimulation by  Leishmania infantum  LPG and/or its lipid and glycan motifs was evaluated with regard to PGE 2  induction. Intact LPG, but not its glycan and lipid moieties, induced a range of proinflammatory responses, including PGE 2  and nitric oxide (NO) release, increased lipid droplet formation, and iNOS and COX2 expression. LPG also induced ERK-1/2 and JNK phosphorylation in macrophages, in addition to the release of PGE 2 , MCP-1, IL-6, TNF-α and IL-12p70, but not IL-10. Pharmacological inhibition of ERK1/2 and PKC affected PGE 2  and cytokine production. Moreover, treatment with rosiglitazone, an agonist of peroxisome proliferator-activated receptor gamma (PPAR-γ), also modulated the release of PGE 2  and other proinflammatory mediators. Finally, we determined that LPG-induced PPAR-γ signaling occurred via TLR1/2. Taken together, these results reinforce the role played by  L .  infantum- derived LPG in the proinflammatory response seen in  Leishmania  infection.

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Leishmania infantum lipophosphoglycan induced-Prostaglandin E2 production in association with PPAR-γ expression via activation of Toll like receptors-1 and 2