Poster

  • P-AE-010

A Drosophila Model for Infection-induced Loss of Intestinal Barrier Function and Homeostasis

Presented in

Poster Session 2

Poster topics

Authors

Nichole Broderick (Baltimore, MD / US)

Abstract

The innate immune response is the first line of defense against infections in both Drosophila melanogaster and humans. In flies, the Toll and immune deficiency (Imd) pathways recognize pathogen-associated molecules, such as peptidoglycan, to activate host immune responses during infection. However, relatively few natural pathogens have been used to study mechanisms of innate immunity in D. melanogaster. To better understand the breadth of host responses to various microbes this study characterizes the response of D. melanogaster to a novel pathogen, Chromobacterium subtsugae, a Gram-negative environmental bacterium known for its quorum sensing production of the purple-pigment violacein. We fed C. subtsugae to adult D. melanogaster and found flies are significantly more susceptible to a purple pigmented strain that over produces violacein, compared to the wild-type non-pigmented strain. Moreover, the infectious process with this violacein producing strain follows defined events. Initially after infection, pathogen load is high and is associated with significant gut damage and the induction of immune and stress response pathways within the first 24 hours. By day 4, almost no C. sustugae can be cultured from flies, but death does not occur until 7-10 days post infection. This uncoupling of pathogen presence and host death, akin to sepsis, provides a unique infection course to study host responses to pathogen-induced damage. Imaging of fly guts over the course of infection indicates that after day 4 dead bacterial cells persist in the gut, which undergoes significant morphological changes as disease progresses. We will discuss our exploration of early events in the course of infection that lead to death and how host immune and stress responses contribute to pathogenesis, as well as microbial factors that elicit these impacts on the host. Altogether, this novel pathogen model provides a useful tool to study how host-microbe interactions can lead to the loss of host homeostasis.

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