Faculty Advisor

Minal Mulye PhD

Document Type


Publication Date



Medicine and Health Sciences


Context: Lipid droplets (LDs) are cytoplasmic lipid storage organelles that have recently gained importance in host-pathogen interactions. They are surrounded by a phospholipid monolayer and store excess cellular free fatty acids and cholesterol as triacylglycerol (TAG) and cholesterol ester (CE) respectively. LDs are crucial to lipid metabolism and energy homeostasis. Further, their role in membrane trafficking, cell signaling, and inflammation make them a prime target for pathogens. Several bacterial, viral, and protozoal pathogens exploit host- or self-derived LDs to build new infectious progeny and/or modulate inflammation to promote infection. However, the diverse role of LDs in different bacterial pathogens remains elusive and merits in-depth elucidation. Objective: The goal of this review is to summarize the current research describing how certain bacterial pathogens manipulate LDs, and how those LDs affect the survival and infectivity of said bacteria. Methods/Design: We investigated literature from the last ten years involving LD-pathogen interactions for the intracellular pathogens Mycobacterium tuberculosis, Mycobacterium leprae, and Mycobacterium bovis; and the extracellular pathogens Pseudomonas aeruginosa and Vibrio cholera. Results: Mycobacterium spp. use LDs as both a fatty acid reservoir and a source of immune mediators, thus enhancing bacterial growth. Pseudomonas mobilizes LDs to increase its virulence whereas V. cholera uses fatty acids derived from aquatic animals to remodel its membrane phospholipids and provide stability for the bacterium. Conclusion: Because LDs are important metabolic organelles, understanding how pathogens exploit LDs during infection will emphasize the underappreciated role of cellular metabolic processes during bacterial infections. Our review will shed light on the importance of LDs during intracellular and extracellular bacterial infections, exploring a novel aspect of host-pathogen interactions.


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