Apr 24, 2012

Infection-induced intestinal oxidative stress triggers organ-to-organ immunological communication in Drosophila

Cell Host & Microbe
Shih-Cheng WuJyh-Lyh Juang

Abstract

Local infections can trigger immune responses in distant organs, and this interorgan immunological crosstalk helps maintain immune homeostasis. We find that enterobacterial infection or chemically and genetically stimulating reactive oxygen species (ROS)-induced stress responses in the Drosophila gut triggers global antimicrobial peptide (AMP) responses in the fat body, a major immune organ in flies. ROS stress induces nitric oxide (NO) production in the gut, which triggers production of the AMP Diptericin, but not Drosomycin, in the fat body. Hemocytes serve as a signaling relay for communication between intestinal ROS/NO signaling and fat body AMP responses. The induction of AMP responses requires Rel/NF-κB activation within the fat body. Although Rel-mediated Drosomycin induction is repressed by the AP-1 transcription factor, this repressor activity is inhibited by intestinal ROS. Thus, intestinal ROS signaling plays an important role in initiating gut-to-fat body immunological communication in Drosophila.

Mentioned in this Paper

Microorganism
JUN gene
JUND gene
Immune Response
Biochemical Pathway
Peptide Growth Factors Deficiency
Fat Pad
Hydrogen Peroxide
Transcription Repressor/Corepressor
NCKAP1 gene

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