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A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken
Previous studies have shown a tissue immune phenotype-altering event occurring on days 2 and 4 in the ceca post-Salmonella challenge. To evaluate the involvement of the cecal microbiota in the phenotype reprogramming, we hypothesized that the addition of subtherapeutic bacitracin (BMD) will affect t...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7760021/ https://www.ncbi.nlm.nih.gov/pubmed/33260977 http://dx.doi.org/10.3390/microorganisms8121879 |
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author | Lee, Annah Bortoluzzi, Cristiano Pilla, Rachel Kogut, Michael H. |
author_facet | Lee, Annah Bortoluzzi, Cristiano Pilla, Rachel Kogut, Michael H. |
author_sort | Lee, Annah |
collection | PubMed |
description | Previous studies have shown a tissue immune phenotype-altering event occurring on days 2 and 4 in the ceca post-Salmonella challenge. To evaluate the involvement of the cecal microbiota in the phenotype reprogramming, we hypothesized that the addition of subtherapeutic bacitracin (BMD) will affect the cecal microbiota. Therefore, the objective of this study was to determine if the antibiotic-mediated changes in the microbiota composition influenced the immune phenotype induced by Salmonella enteritidis infection of the chicken cecum. A total of 112 fertile eggs were obtained for each experiment, repeated for a total of three separate times. The ceca and cecal contents were collected on days 2 and 4 post-infection for mRNA expression TaqMan assay and 16S rRNA gene microbiota sequencing. The results demonstrate the effects of bacitracin on cecal composition and its interaction with Salmonella enteritidis in young chicks. There is a preliminary indication of phenotype change in the Salmonella-challenged group provided subtherapeutic BMD due to the shifting cecal microbiota and cecal immune response, indicating the addition of bacitracin during infection altered the cecal phenotype. These data demonstrate the potential involvement of the microbiota in reprogramming immune phenotype (disease resistance to disease tolerance) induced by Salmonella in the chicken cecum. |
format | Online Article Text |
id | pubmed-7760021 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-77600212020-12-26 A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken Lee, Annah Bortoluzzi, Cristiano Pilla, Rachel Kogut, Michael H. Microorganisms Article Previous studies have shown a tissue immune phenotype-altering event occurring on days 2 and 4 in the ceca post-Salmonella challenge. To evaluate the involvement of the cecal microbiota in the phenotype reprogramming, we hypothesized that the addition of subtherapeutic bacitracin (BMD) will affect the cecal microbiota. Therefore, the objective of this study was to determine if the antibiotic-mediated changes in the microbiota composition influenced the immune phenotype induced by Salmonella enteritidis infection of the chicken cecum. A total of 112 fertile eggs were obtained for each experiment, repeated for a total of three separate times. The ceca and cecal contents were collected on days 2 and 4 post-infection for mRNA expression TaqMan assay and 16S rRNA gene microbiota sequencing. The results demonstrate the effects of bacitracin on cecal composition and its interaction with Salmonella enteritidis in young chicks. There is a preliminary indication of phenotype change in the Salmonella-challenged group provided subtherapeutic BMD due to the shifting cecal microbiota and cecal immune response, indicating the addition of bacitracin during infection altered the cecal phenotype. These data demonstrate the potential involvement of the microbiota in reprogramming immune phenotype (disease resistance to disease tolerance) induced by Salmonella in the chicken cecum. MDPI 2020-11-27 /pmc/articles/PMC7760021/ /pubmed/33260977 http://dx.doi.org/10.3390/microorganisms8121879 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Lee, Annah Bortoluzzi, Cristiano Pilla, Rachel Kogut, Michael H. A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title | A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title_full | A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title_fullStr | A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title_full_unstemmed | A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title_short | A Role for the Microbiota in the Immune Phenotype Alteration Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken |
title_sort | role for the microbiota in the immune phenotype alteration associated with the induction of disease tolerance and persistent asymptomatic infection of salmonella in the chicken |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7760021/ https://www.ncbi.nlm.nih.gov/pubmed/33260977 http://dx.doi.org/10.3390/microorganisms8121879 |
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