Frontiers in Molecular Biosciences · 2 authors, 2 centres
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This narrative review examines how intracellular pathogens hijack host lipid metabolism pathways—particularly those involving LCAT and LPL enzymes—and discusses the opportunities and risks of host-directed therapeutic strategies that target these shared metabolic processes.
This narrative review by Konaklieva and Plotkin synthesizes existing literature on host-directed therapy (HDT) as an emerging anti-infective strategy targeting host cell lipid metabolism exploited by intracellular pathogens. The authors describe how facultative and obligate intracellular pathogens regulate host exogenous lipid uptake and expression of host lipid biosynthesis enzymes to support replication. A central theme is that pathogens either hijack mammalian lipid enzymes or produce their own analogous versions of LCAT and LPL, thereby interfering with human lipid metabolism. The review links these mechanisms to cardiovascular disease, noting that HDL-C levels are inversely related to CVD risk and that LCAT is critical for HDL particle maturation. The authors caution that lipid-lowering therapeutics, including LCAT activators and LPL-modulating agents, may have unintended secondary effects on host-pathogen interactions. They cite evidence that β-lactam antibiotics trigger MRSA production of LPL, promoting increased virulence.
