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Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
Yersinia pestis, the causative agent of bubonic and pneumonic plague, is typically a zoonotic vector-borne disease of wild rodents. Bacterial biofilm formation in the proventriculus of the flea contributes to chronic infection of fleas and facilitates efficient disease transmission. However prior to...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4503695/ https://www.ncbi.nlm.nih.gov/pubmed/26177454 http://dx.doi.org/10.1371/journal.pone.0133318 |
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author | Earl, Shaun C. Rogers, Miles T. Keen, Jennifer Bland, David M. Houppert, Andrew S. Miller, Caitlynn Temple, Ian Anderson, Deborah M. Marketon, Melanie M. |
author_facet | Earl, Shaun C. Rogers, Miles T. Keen, Jennifer Bland, David M. Houppert, Andrew S. Miller, Caitlynn Temple, Ian Anderson, Deborah M. Marketon, Melanie M. |
author_sort | Earl, Shaun C. |
collection | PubMed |
description | Yersinia pestis, the causative agent of bubonic and pneumonic plague, is typically a zoonotic vector-borne disease of wild rodents. Bacterial biofilm formation in the proventriculus of the flea contributes to chronic infection of fleas and facilitates efficient disease transmission. However prior to biofilm formation, ingested bacteria must survive within the flea midgut, and yet little is known about vector-pathogen interactions that are required for flea gut colonization. Here we establish a Drosophila melanogaster model system to gain insight into Y. pestis colonization of the insect vector. We show that Y. pestis establishes a stable infection in the anterior midgut of fly larvae, and we used this model system to study the roles of genes involved in biofilm production and/or resistance to gut immunity stressors. We find that PhoP and GmhA both contribute to colonization and resistance to antimicrobial peptides in flies, and furthermore, the data suggest biofilm formation may afford protection against antimicrobial peptides. Production of reactive oxygen species in the fly gut, as in fleas, also serves to limit bacterial infection, and OxyR mediates Y. pestis survival in both insect models. Overall, our data establish the fruit fly as an informative model to elucidate the relationship between Y. pestis and its flea vector. |
format | Online Article Text |
id | pubmed-4503695 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-45036952015-07-17 Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis Earl, Shaun C. Rogers, Miles T. Keen, Jennifer Bland, David M. Houppert, Andrew S. Miller, Caitlynn Temple, Ian Anderson, Deborah M. Marketon, Melanie M. PLoS One Research Article Yersinia pestis, the causative agent of bubonic and pneumonic plague, is typically a zoonotic vector-borne disease of wild rodents. Bacterial biofilm formation in the proventriculus of the flea contributes to chronic infection of fleas and facilitates efficient disease transmission. However prior to biofilm formation, ingested bacteria must survive within the flea midgut, and yet little is known about vector-pathogen interactions that are required for flea gut colonization. Here we establish a Drosophila melanogaster model system to gain insight into Y. pestis colonization of the insect vector. We show that Y. pestis establishes a stable infection in the anterior midgut of fly larvae, and we used this model system to study the roles of genes involved in biofilm production and/or resistance to gut immunity stressors. We find that PhoP and GmhA both contribute to colonization and resistance to antimicrobial peptides in flies, and furthermore, the data suggest biofilm formation may afford protection against antimicrobial peptides. Production of reactive oxygen species in the fly gut, as in fleas, also serves to limit bacterial infection, and OxyR mediates Y. pestis survival in both insect models. Overall, our data establish the fruit fly as an informative model to elucidate the relationship between Y. pestis and its flea vector. Public Library of Science 2015-07-15 /pmc/articles/PMC4503695/ /pubmed/26177454 http://dx.doi.org/10.1371/journal.pone.0133318 Text en https://creativecommons.org/publicdomain/zero/1.0/ This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. |
spellingShingle | Research Article Earl, Shaun C. Rogers, Miles T. Keen, Jennifer Bland, David M. Houppert, Andrew S. Miller, Caitlynn Temple, Ian Anderson, Deborah M. Marketon, Melanie M. Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis |
title | Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
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title_full | Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
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title_fullStr | Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
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title_full_unstemmed | Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
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title_short | Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis
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title_sort | resistance to innate immunity contributes to colonization of the insect gut by yersinia pestis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4503695/ https://www.ncbi.nlm.nih.gov/pubmed/26177454 http://dx.doi.org/10.1371/journal.pone.0133318 |
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