Abstract
Local infections can trigger immune responses in distant organs and this inter-organ immunological cross-talk helps maintain immune homeostasis. However, the molecular mechanism underlying this inter-organ immune communication still remains unclear. Previous studies by others have shown that Drosophila larvae orally infected with enterobacteria Ecc15 (Erwinia carotovora subsp.) triggers systemic antimicrobial peptides (AMPs) response in fat body, the functional counterpart of mammalian liver. We find that enterobacterial infection or chemically and genetically stimulating reactive oxygen species (ROS)-induced stress responses in the Drosophila gut triggers global AMP responses in the fat body. Further genetic and chemical experiments suggest that ROS stress induces nitric oxide (NO) production in the gut, which triggers production of the AMP Diptericin, but not Drosomycin, in the fat body. In addition, hemocytes serve as a signaling relay for communication between intestinal ROS/NO signaling and Rel/NF-kB-dependent AMP responses in fat body. We also find transcription factor AP-1 repressed AMP expressions in fat body but this repressor activity is inhibited by intestinal ROS stress. Taken together, our data suggest that intestinal ROS signaling plays an important role in initiating gut-to-fat body immunological communication in Drosophila.