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Host and microbial lipid metabolism pathways encompass the integrated biochemical network where human metabolic processes interact with those of the resident or pathogenic microbiota [6, 13]. This system involves the microbial transformation of dietary and host-derived lipids into bioactive metabolites, such as secondary bile acids and short-chain fatty acids (SCFAs), which modulate host physiology through receptors like the farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) [13, 16]. In the context of infectious diseases, pathogens such as Mycobacterium tuberculosis and various viruses (e.g., HCV, SARS-CoV-2) hijack host lipid synthesis and storage organelles, such as lipid droplets, to facilitate their replication, assembly, and immune evasion [1, 3, 10]. Therapeutic strategies targeting these pathways include host-directed therapies (HDTs) that inhibit host enzymes like diacylglycerol acyltransferase 1 (DGAT1) or acid sphingomyelinase (ASM) to deprive pathogens of nutrients or disrupt their life cycle [2, 4, 7]. Additionally, modulating the gut-liver axis through microbiome-targeted interventions is being explored to treat metabolic disorders like dyslipidemia and colorectal cancer [5, 8]. Consequently, this metabolic interface represents a critical area for developing broad-spectrum antimicrobials and therapies for chronic metabolic diseases [14, 15].
Inhibition of host or microbial lipid biosynthesis, modulation of bile acid signaling via host receptors, and nutrient deprivation of intracellular pathogens.
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