ArticleBMC microbiology2026
Drosophila melanogaster mitigates gastro-oral infections by stimulating pathogen expulsion.
Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
backgroundFood-borne pathogens, particularly belonging to the Enterobacteriaceae family, are a major cause of gastrointestinal infections in humans. While Drosophila melanogaster has been widely explored to study antimicrobial responses, most studies rely on septic injury or direct injection routes that bypass the gut. A coordinated set of antimicrobial defenses acts to counteract the invading bacteria, with some variations depending on the entry route into the host. Herein, we tracked the dynamics of Enterobacteriaceae pathogens in Drosophila using a natural infection route.
resultsMost bacterial species were cleared within 48 h post-infection (hpi). We did not observe any significant mortality, indicating robust infection control. At 4 hpi, a substantial increase in reactive oxygen species (ROS) production was observed, followed by a decrease at 24 hpi and a resurgence at 48 hpi. We further show that bacteria were expelled by the fly, possibly due to TRPA1 induction, a ROS-sensing receptor. Although the infected dual oxidase (Duox) knockdown flies showed no difference in survival rate compared to the uninfected ones, they showed differential TRPA1 induction and pathogen expulsion, suggesting that ROS alone is insufficient for TRPA1 induction and infection control.
conclusionsOur findings reveal that the host can distinguish and respond to various bacterial species in a well-synchronized, gut-localized, and pathogen-specific manner. This also illustrates the reliability of natural infection route models in unravelling and understanding the complexities of host-pathogen interaction.
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