No blood, no guts, no glory: the Drosophila gut-immune axis during injury

Tissue damage is a significant threat to organisms, resulting from infections or injuries. Animals have evolved mechanisms to recognize damage-associated molecular patterns (DAMPs) and activate pathways for repair and inflammation. However, the molecular mechanisms and cellular responses to DAMPs remain poorly understood. In this study, blood cell gene expression profiles were analyzed at injury sites in flies. The upregulation of JAK/STAT cytokine upd-3 (IL-6) and the Toll pathway, typically associated with pathogen infection, was observed. Intracellular accumulation of hydrogen peroxide and its import into blood cells via the water channel Prip were found to be crucial for upd-3 induction post-injury. Impairment of cytokine upd-3 production was observed in blood cells lacking Prip. Interestingly, injury-based activation of blood cells enhanced protection against Enterococcus faecalis infection, dependent on hydrogen peroxide production at the injury site.

The gut houses a large portion of immune cells in humans and plays a vital role in nutrient absorption. Previous research demonstrated that blood cells in flies act as messengers between injury sites and the intestine to regulate stem cell proliferation. Failure of blood cell activation and hydrogen peroxide signaling post-injury led to inhibited intestinal stem cell proliferation and increased susceptibility to injury. My research aims to uncover the molecular mechanisms underlying intestinal stem cell proliferation triggered by thoracic injury in Drosophila