Related Experiment Video
Updated: Jul 9, 2026

Systemic Bacterial Infection and Immune Defense Phenotypes in Drosophila Melanogaster
Published on: May 13, 2015
A model of bacterial intestinal infections in Drosophila melanogaster
Nadine T Nehme1, Samuel Liégeois, Beatrix Kele
1Equipe Fondation Recherche Médicale, UPR 9022 du CNRS, Institut de Biologie Moléculaire et Cellulaire du CNRS, Strasbourg, France.
Abstract:
Serratia marcescens is an entomopathogenic bacterium that opportunistically infects a wide range of hosts, including humans. In a model of septic injury, if directly introduced into the body cavity of Drosophila, this pathogen is insensitive to the host's systemic immune response and kills flies in a day. We find that S. marcescens resistance to the Drosophila immune deficiency (imd)-mediated humoral response requires the bacterial lipopolysaccharide O-antigen. If ingested by Drosophila, bacteria cross the gut and penetrate the body cavity. During this passage, the bacteria can be observed within the cells of the intestinal epithelium. In such an oral infection model, the flies succumb to infection only after 6 days. We demonstrate that two complementary host defense mechanisms act together against such food-borne infection: an antimicrobial response in the intestine that is regulated by the imd pathway and phagocytosis by hemocytes of bacteria that have escaped into the hemolymph. Interestingly, bacteria present in the hemolymph elicit a systemic immune response only when phagocytosis is blocked. Our observations support a model wherein peptidoglycan fragments released during bacterial growth activate the imd pathway and do not back a proposed role for phagocytosis in the immune activation of the fat body. Thanks to the genetic tools available in both host and pathogen, the molecular dissection of the interactions between S. marcescens and Drosophila will provide a useful paradigm for deciphering intestinal pathogenesis.
Insights
Serratia marcescens evades the Drosophila immune deficiency (imd) pathway via its O-antigen. Oral infection triggers intestinal immunity and hemocyte phagocytosis, crucial for host survival against this opportunistic pathogen.
Area of Science:
- Microbiology
- Immunology
- Infectious Disease
Background:
- Serratia marcescens is an opportunistic pathogen infecting diverse hosts, including humans.
- In Drosophila, direct injection leads to rapid death, indicating evasion of systemic immunity.
Purpose of the Study:
- Investigate the mechanisms of S. marcescens pathogenesis in Drosophila.
- Elucidate host immune responses to oral S. marcescens infection.
Main Methods:
- Utilized Drosophila melanogaster as a model organism.
- Administered S. marcescens orally and via injection.
- Analyzed immune responses including the imd pathway and hemocyte activity.
Main Results:
- S. marcescens resistance to the imd pathway requires its lipopolysaccharide O-antigen.
- Oral infection involves gut penetration and delayed mortality (6 days).
- Dual defense mechanisms—intestinal imd-regulated antimicrobial response and hemocyte phagocytosis—protect against oral infection.
Conclusions:
- The bacterial O-antigen is critical for evading the Drosophila immune deficiency (imd) pathway.
- Intestinal and hemolymph-based immunity are complementary defenses against food-borne S. marcescens.
- This host-pathogen interaction provides a model for studying intestinal pathogenesis.

