Acute exposure of Nicotine during Drosophila puncture injury activates an epidermal wound response reaction.

Epidermal wound reaction after injury can be visualized in Drosophila melanogaster embryos by transgenic fluorescent wound reporters. A “local” reaction is limited to the epidermal cells surrounding a wound site occurs in wildtype embryos. A “global” reaction extends beyond the wound site to all epidermal cells occurs in immune response mutants (e.g. Flotillin-2 and Toll). The aim of this investigation is to explore the effect of nicotine on the localization of Drosophila wound reaction. Nicotine may have the potential to negatively affect wound repair by inhibiting a local reaction, and ultimately impeding epidermal wound recovery in Drosophila. We find nicotine exposure activates a global reaction after puncture injury of Drosophila embryos. Determining the effect of nicotine exposure on wound reaction in Drosophila may lead to improved understanding of how nicotine use in humans may influence wound healing after tissue damage.