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Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam
Gut microbiota depletion is a pivotal prerequisite to warrant Campylobacter jejuni infection and induced inflammation in IL-10(-/-) mice used as acute campylobacteriosis model. We here assessed the impact of an 8-week antibiotic regimen of ampicillin, ciprofloxacin, imipenem, metronidazole, and vanc...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Akadémiai Kiadó
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9530677/ https://www.ncbi.nlm.nih.gov/pubmed/36069779 http://dx.doi.org/10.1556/1886.2022.00014 |
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author | Heimesaat, Markus M. Mousavi, Soraya Bandick, Rasmus Bereswill, Stefan |
author_facet | Heimesaat, Markus M. Mousavi, Soraya Bandick, Rasmus Bereswill, Stefan |
author_sort | Heimesaat, Markus M. |
collection | PubMed |
description | Gut microbiota depletion is a pivotal prerequisite to warrant Campylobacter jejuni infection and induced inflammation in IL-10(-/-) mice used as acute campylobacteriosis model. We here assessed the impact of an 8-week antibiotic regimen of ampicillin, ciprofloxacin, imipenem, metronidazole, and vancomycin (ABx) as compared to ampicillin plus sulbactam (A/S) on gut microbiota depletion and immunopathological responses upon oral C. jejuni infection. Our obtained results revealed that both antibiotic regimens were comparably effective in depleting the murine gut microbiota facilitating similar pathogenic colonization alongside the gastrointestinal tract following oral infection. Irrespective of the preceding microbiota depletion regimen, mice were similarly compromised by acute C. jejuni induced enterocolitis as indicated by comparable clinical scores and macroscopic as well as microscopic sequelae such as colonic histopathology and apoptosis on day 6 post-infection. Furthermore, innate and adaptive immune cell responses in the large intestines were similar in both infected cohorts, which also held true for intestinal, extra-intestinal and even systemic secretion of pro-inflammatory cytokines such as TNF-α, IFN-γ, and IL-6. In conclusion, gut microbiota depletion in IL-10(-/-) mice by ampicillin plus sulbactam is sufficient to investigate both, C. jejuni infection and the immunopathological features of acute campylobacteriosis. |
format | Online Article Text |
id | pubmed-9530677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Akadémiai Kiadó |
record_format | MEDLINE/PubMed |
spelling | pubmed-95306772022-10-17 Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam Heimesaat, Markus M. Mousavi, Soraya Bandick, Rasmus Bereswill, Stefan Eur J Microbiol Immunol (Bp) Article Gut microbiota depletion is a pivotal prerequisite to warrant Campylobacter jejuni infection and induced inflammation in IL-10(-/-) mice used as acute campylobacteriosis model. We here assessed the impact of an 8-week antibiotic regimen of ampicillin, ciprofloxacin, imipenem, metronidazole, and vancomycin (ABx) as compared to ampicillin plus sulbactam (A/S) on gut microbiota depletion and immunopathological responses upon oral C. jejuni infection. Our obtained results revealed that both antibiotic regimens were comparably effective in depleting the murine gut microbiota facilitating similar pathogenic colonization alongside the gastrointestinal tract following oral infection. Irrespective of the preceding microbiota depletion regimen, mice were similarly compromised by acute C. jejuni induced enterocolitis as indicated by comparable clinical scores and macroscopic as well as microscopic sequelae such as colonic histopathology and apoptosis on day 6 post-infection. Furthermore, innate and adaptive immune cell responses in the large intestines were similar in both infected cohorts, which also held true for intestinal, extra-intestinal and even systemic secretion of pro-inflammatory cytokines such as TNF-α, IFN-γ, and IL-6. In conclusion, gut microbiota depletion in IL-10(-/-) mice by ampicillin plus sulbactam is sufficient to investigate both, C. jejuni infection and the immunopathological features of acute campylobacteriosis. Akadémiai Kiadó 2022-09-07 2022-09 /pmc/articles/PMC9530677/ /pubmed/36069779 http://dx.doi.org/10.1556/1886.2022.00014 Text en © 2022 The Author(s) https://creativecommons.org/licenses/by-nc/4.0/ Open Access. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated. |
spellingShingle | Article Heimesaat, Markus M. Mousavi, Soraya Bandick, Rasmus Bereswill, Stefan Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title |
Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title_full |
Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title_fullStr |
Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title_full_unstemmed |
Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title_short |
Campylobacter jejuni infection induces acute enterocolitis in IL-10(-/-) mice pretreated with ampicillin plus sulbactam |
title_sort | campylobacter jejuni infection induces acute enterocolitis in il-10(-/-) mice pretreated with ampicillin plus sulbactam |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9530677/ https://www.ncbi.nlm.nih.gov/pubmed/36069779 http://dx.doi.org/10.1556/1886.2022.00014 |
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