ABSTRACT
Lipid droplets (LDs) are dynamic intracellular organelles critical for lipid metabolism. Dynamic alterations in the configurations and functions of LDs during innate immune response to bacterial infections and the underlying mechanisms however, remain largely unknown. Herein, we trace the time-course morphology of LDs in fat bodies of Drosophila after transient bacterial infection. Detailed analysis shows that perilipin1 (plin1), a core gene regulating lipid metabolism of LDs is suppressed by IMD/Relish, an innate immune signaling. During immune activation, downregulated plin1 promotes the enlargement of LDs, which in turn alleviates immune reaction-associated reactive oxygen species (ROS) stress. Thus, the growth of LDs is likely an active adaptation to maintain redox homeostasis in response to IMD activation. Therefore, our study provides evidence that plin1 serves as a modulator on LDs’ reconfiguration in regulating infection-induced pathogenesis, and Plin1 might be a potential therapeutic target for coordinating inflammation resolution and lipid metabolism.
Competing Interest Statement
The authors have declared no competing interest.
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