Accumulation of lipid droplets induced by Listeria monocytogenes in macrophages: implications for survival and evasion of innate immunity.

Abstract

Listeriosis, caused by Listeria monocytogenes (L.m.), poses a significant public health concern as one of the most severe foodborne diseases. The pathogenesis of L.m. involves critical steps such as phagosome rupture and escape upon internalization. Throughout infection, L.m. influences various host processes, including lipid metabolism pathways, yet the role of lipid droplets (LDs) remains unclear. Here, we reported a rapid, time-dependent increase in LD formation in macrophages induced by L.m. LD biogenesis was found to be dependent on L.m. viability and virulence genes, particularly on the activity of the pore-forming protein listeriolysin O (LLO). The prevention of LD formation by inhibiting diacylglycerol O-acyltransferase 1 (DGAT1) and cytosolic phospholipase A2 (cPLA2) significantly reduced intracellular bacterial survival, impaired prostaglandin E2 synthesis, and decreased interleukin-10 production. Additionally, inhibiting LD formation led to increased levels of tumor necrosis factor α and interferon β. Collectively, our data suggest a role for LDs in promoting L.m. cell survival and evasion within macrophages.