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Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD
BACKGROUND: Intestinal bacteria are thought to play a role in the pathogenesis of human inflammatory bowel disease (IBD). We investigated whether oral inoculation with specific intestinal bacteria increased colon inflammation in the multi-drug resistance 1a-deficient (Mdr1a(–/–)) mouse model of IBD....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778357/ https://www.ncbi.nlm.nih.gov/pubmed/26940566 http://dx.doi.org/10.1186/s12876-016-0447-y |
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author | Barnett, Matthew P. G. Dommels, Yvonne E. M. Butts, Christine A. Zhu, Shuotun McNabb, Warren C. Roy, Nicole C. |
author_facet | Barnett, Matthew P. G. Dommels, Yvonne E. M. Butts, Christine A. Zhu, Shuotun McNabb, Warren C. Roy, Nicole C. |
author_sort | Barnett, Matthew P. G. |
collection | PubMed |
description | BACKGROUND: Intestinal bacteria are thought to play a role in the pathogenesis of human inflammatory bowel disease (IBD). We investigated whether oral inoculation with specific intestinal bacteria increased colon inflammation in the multi-drug resistance 1a-deficient (Mdr1a(–/–)) mouse model of IBD. METHODS: Five-week-old Mdr1a(–/–) mice (FVB background) and FVB mice were randomly assigned to one of two treatment groups (Control or Inoculation, n = 12 per group). All mice were fed AIN-76A rodent diet, and mice in the Inoculation groups also received a single oral bacterial inoculation consisting of twelve cultured Enterococcus species combined with conventional intestinal flora obtained from the gastrointestinal tract of healthy mice (EF.CIF). Body weight, food intake, and disease activity index (DAI) were assessed throughout the study, and at 21 or 24 weeks of age, inflammation was assessed post-mortem by determining colon length and histological injury score (HIS), and plasma serum amyloid A (SAA). RESULTS: Mdr1a(–/–) mice consumed more food than FVB mice at 13 weeks of age (P < 0.05). There was also a significant effect of genotype on body weight, with Mdr1a(–/–) mice weighing less than FVB mice throughout the study (P < 0.05) regardless of treatment, but there was no effect of inoculation on body weight (P > 0.25). Colon HIS of Mdr1a(–/–) mice was significantly higher than that of FVB mice in the Control (9.3 ± 4.7 (mean ± SD) vs. 0.58 ± 0.51; P < 0.001) and Inoculation (6.7 ± 5.1 vs. 0.92 ± 0.39; P < 0.001) groups. There was no difference in colon HIS of Mdr1a(–/–) mice in the Control group compared with Mdr1a(–/–) mice in the Inoculation group (P = 0.25), nor was there any difference in within-group variation of colon HIS in these two Mdr1a(–/–) groups. DAI was higher in Mdr1a(–/–) mice than in FVB mice, but there was no effect of treatment in either strain, nor were there any differences in colon length or plasma SAA. CONCLUSIONS: Inoculation of Mdr1a(–/–) mice with the EF.CIF inoculum described here does not increase colon inflammation or reduce the observed variability of inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12876-016-0447-y) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4778357 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-47783572016-03-05 Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD Barnett, Matthew P. G. Dommels, Yvonne E. M. Butts, Christine A. Zhu, Shuotun McNabb, Warren C. Roy, Nicole C. BMC Gastroenterol Research Article BACKGROUND: Intestinal bacteria are thought to play a role in the pathogenesis of human inflammatory bowel disease (IBD). We investigated whether oral inoculation with specific intestinal bacteria increased colon inflammation in the multi-drug resistance 1a-deficient (Mdr1a(–/–)) mouse model of IBD. METHODS: Five-week-old Mdr1a(–/–) mice (FVB background) and FVB mice were randomly assigned to one of two treatment groups (Control or Inoculation, n = 12 per group). All mice were fed AIN-76A rodent diet, and mice in the Inoculation groups also received a single oral bacterial inoculation consisting of twelve cultured Enterococcus species combined with conventional intestinal flora obtained from the gastrointestinal tract of healthy mice (EF.CIF). Body weight, food intake, and disease activity index (DAI) were assessed throughout the study, and at 21 or 24 weeks of age, inflammation was assessed post-mortem by determining colon length and histological injury score (HIS), and plasma serum amyloid A (SAA). RESULTS: Mdr1a(–/–) mice consumed more food than FVB mice at 13 weeks of age (P < 0.05). There was also a significant effect of genotype on body weight, with Mdr1a(–/–) mice weighing less than FVB mice throughout the study (P < 0.05) regardless of treatment, but there was no effect of inoculation on body weight (P > 0.25). Colon HIS of Mdr1a(–/–) mice was significantly higher than that of FVB mice in the Control (9.3 ± 4.7 (mean ± SD) vs. 0.58 ± 0.51; P < 0.001) and Inoculation (6.7 ± 5.1 vs. 0.92 ± 0.39; P < 0.001) groups. There was no difference in colon HIS of Mdr1a(–/–) mice in the Control group compared with Mdr1a(–/–) mice in the Inoculation group (P = 0.25), nor was there any difference in within-group variation of colon HIS in these two Mdr1a(–/–) groups. DAI was higher in Mdr1a(–/–) mice than in FVB mice, but there was no effect of treatment in either strain, nor were there any differences in colon length or plasma SAA. CONCLUSIONS: Inoculation of Mdr1a(–/–) mice with the EF.CIF inoculum described here does not increase colon inflammation or reduce the observed variability of inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12876-016-0447-y) contains supplementary material, which is available to authorized users. BioMed Central 2016-03-03 /pmc/articles/PMC4778357/ /pubmed/26940566 http://dx.doi.org/10.1186/s12876-016-0447-y Text en © Barnett et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Barnett, Matthew P. G. Dommels, Yvonne E. M. Butts, Christine A. Zhu, Shuotun McNabb, Warren C. Roy, Nicole C. Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title | Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title_full | Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title_fullStr | Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title_full_unstemmed | Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title_short | Inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of IBD |
title_sort | inoculation with enterococci does not affect colon inflammation in the multi-drug resistance 1a-deficient mouse model of ibd |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778357/ https://www.ncbi.nlm.nih.gov/pubmed/26940566 http://dx.doi.org/10.1186/s12876-016-0447-y |
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