A model of bacterial intestinal infections in Drosophila melanogaster.

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 flie...

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Autores principales:	Nadine T Nehme, Samuel Liégeois, Beatrix Kele, Philippe Giammarinaro, Elizabeth Pradel, Jules A Hoffmann, Jonathan J Ewbank, Dominique Ferrandon
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2007
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/6ecbbce927434b26a38c5fecb8876bcd
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id	oai:doaj.org-article:6ecbbce927434b26a38c5fecb8876bcd
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spelling	oai:doaj.org-article:6ecbbce927434b26a38c5fecb8876bcd2021-11-25T05:46:50ZA model of bacterial intestinal infections in Drosophila melanogaster.1553-73661553-737410.1371/journal.ppat.0030173https://doaj.org/article/6ecbbce927434b26a38c5fecb8876bcd2007-11-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.0030173https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Serratia 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.Nadine T NehmeSamuel LiégeoisBeatrix KelePhilippe GiammarinaroElizabeth PradelJules A HoffmannJonathan J EwbankDominique FerrandonPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 3, Iss 11, p e173 (2007)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Nadine T Nehme Samuel Liégeois Beatrix Kele Philippe Giammarinaro Elizabeth Pradel Jules A Hoffmann Jonathan J Ewbank Dominique Ferrandon A model of bacterial intestinal infections in Drosophila melanogaster.
description	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.
format	article
author	Nadine T Nehme Samuel Liégeois Beatrix Kele Philippe Giammarinaro Elizabeth Pradel Jules A Hoffmann Jonathan J Ewbank Dominique Ferrandon
author_facet	Nadine T Nehme Samuel Liégeois Beatrix Kele Philippe Giammarinaro Elizabeth Pradel Jules A Hoffmann Jonathan J Ewbank Dominique Ferrandon
author_sort	Nadine T Nehme
title	A model of bacterial intestinal infections in Drosophila melanogaster.
title_short	A model of bacterial intestinal infections in Drosophila melanogaster.
title_full	A model of bacterial intestinal infections in Drosophila melanogaster.
title_fullStr	A model of bacterial intestinal infections in Drosophila melanogaster.
title_full_unstemmed	A model of bacterial intestinal infections in Drosophila melanogaster.
title_sort	model of bacterial intestinal infections in drosophila melanogaster.
publisher	Public Library of Science (PLoS)
publishDate	2007
url	https://doaj.org/article/6ecbbce927434b26a38c5fecb8876bcd
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A model of bacterial intestinal infections in Drosophila melanogaster.

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