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Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken

Salmonella Enteritidis causes fowl paratyphoid in poultry and is frequently associated to outbreaks of food-borne diseases in humans. The role of flagella and flagella-mediated motility into host-pathogen interplay is not fully understood and requires further investigation. In this study, one-day-ol...

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Autores principales: Barbosa, Fernanda de Oliveira, Freitas Neto, Oliveiro Caetano de, Batista, Diego Felipe Alves, Almeida, Adriana Maria de, Rubio, Marcela da Silva, Alves, Lucas Bocchini Rodrigues, Vasconcelos, Rosemeire de Oliveira, Barrow, Paul Andrew, Berchieri Junior, Angelo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628309/
https://www.ncbi.nlm.nih.gov/pubmed/28648636
http://dx.doi.org/10.1016/j.bjm.2017.01.012
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author Barbosa, Fernanda de Oliveira
Freitas Neto, Oliveiro Caetano de
Batista, Diego Felipe Alves
Almeida, Adriana Maria de
Rubio, Marcela da Silva
Alves, Lucas Bocchini Rodrigues
Vasconcelos, Rosemeire de Oliveira
Barrow, Paul Andrew
Berchieri Junior, Angelo
author_facet Barbosa, Fernanda de Oliveira
Freitas Neto, Oliveiro Caetano de
Batista, Diego Felipe Alves
Almeida, Adriana Maria de
Rubio, Marcela da Silva
Alves, Lucas Bocchini Rodrigues
Vasconcelos, Rosemeire de Oliveira
Barrow, Paul Andrew
Berchieri Junior, Angelo
author_sort Barbosa, Fernanda de Oliveira
collection PubMed
description Salmonella Enteritidis causes fowl paratyphoid in poultry and is frequently associated to outbreaks of food-borne diseases in humans. The role of flagella and flagella-mediated motility into host-pathogen interplay is not fully understood and requires further investigation. In this study, one-day-old chickens were challenged orally with a wild-type strain Salmonella Enteritidis, a non-motile but fully flagellated (SE ΔmotB) or non-flagellated (SE ΔfliC) strain to evaluate their ability to colonise the intestine and spread systemically and also of eliciting gross and histopathological changes. SE ΔmotB and SE ΔfliC were recovered in significantly lower numbers from caecal contents in comparison with Salmonella Enteritidis at early stages of infection (3 and 5 dpi). The SE ΔmotB strain, which synthesises paralysed flagella, showed poorer intestinal colonisation ability than the non-flagellated SE ΔfliC. Histopathological analyses demonstrated that the flagellated strains induced more intense lymphoid reactivity in liver, ileum and caeca. Thus, in the present study the flagellar structure and motility seemed to play a role in the early stages of the intestinal colonisation by Salmonella Enteritidis in the chicken.
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spelling pubmed-56283092017-10-10 Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken Barbosa, Fernanda de Oliveira Freitas Neto, Oliveiro Caetano de Batista, Diego Felipe Alves Almeida, Adriana Maria de Rubio, Marcela da Silva Alves, Lucas Bocchini Rodrigues Vasconcelos, Rosemeire de Oliveira Barrow, Paul Andrew Berchieri Junior, Angelo Braz J Microbiol Research Paper Salmonella Enteritidis causes fowl paratyphoid in poultry and is frequently associated to outbreaks of food-borne diseases in humans. The role of flagella and flagella-mediated motility into host-pathogen interplay is not fully understood and requires further investigation. In this study, one-day-old chickens were challenged orally with a wild-type strain Salmonella Enteritidis, a non-motile but fully flagellated (SE ΔmotB) or non-flagellated (SE ΔfliC) strain to evaluate their ability to colonise the intestine and spread systemically and also of eliciting gross and histopathological changes. SE ΔmotB and SE ΔfliC were recovered in significantly lower numbers from caecal contents in comparison with Salmonella Enteritidis at early stages of infection (3 and 5 dpi). The SE ΔmotB strain, which synthesises paralysed flagella, showed poorer intestinal colonisation ability than the non-flagellated SE ΔfliC. Histopathological analyses demonstrated that the flagellated strains induced more intense lymphoid reactivity in liver, ileum and caeca. Thus, in the present study the flagellar structure and motility seemed to play a role in the early stages of the intestinal colonisation by Salmonella Enteritidis in the chicken. Elsevier 2017-06-07 /pmc/articles/PMC5628309/ /pubmed/28648636 http://dx.doi.org/10.1016/j.bjm.2017.01.012 Text en © 2017 Sociedade Brasileira de Microbiologia. Published by Elsevier Editora Ltda. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Paper
Barbosa, Fernanda de Oliveira
Freitas Neto, Oliveiro Caetano de
Batista, Diego Felipe Alves
Almeida, Adriana Maria de
Rubio, Marcela da Silva
Alves, Lucas Bocchini Rodrigues
Vasconcelos, Rosemeire de Oliveira
Barrow, Paul Andrew
Berchieri Junior, Angelo
Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title_full Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title_fullStr Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title_full_unstemmed Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title_short Contribution of flagella and motility to gut colonisation and pathogenicity of Salmonella Enteritidis in the chicken
title_sort contribution of flagella and motility to gut colonisation and pathogenicity of salmonella enteritidis in the chicken
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628309/
https://www.ncbi.nlm.nih.gov/pubmed/28648636
http://dx.doi.org/10.1016/j.bjm.2017.01.012
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