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Primary murine mucosal response during cephalosporin‐induced intestinal colonization by Enterococcus faecium
Hospitalized patients are often administered antibiotics that perturb the gastrointestinal commensal microbiota, leading to outgrowth of antibiotic‐resistant bacteria, like multidrug‐resistant Enterococcus faecium, subsequent spread, and eventually infections. However, the events that occur at the i...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6182561/ https://www.ncbi.nlm.nih.gov/pubmed/29484836 http://dx.doi.org/10.1002/mbo3.602 |
Sumario: | Hospitalized patients are often administered antibiotics that perturb the gastrointestinal commensal microbiota, leading to outgrowth of antibiotic‐resistant bacteria, like multidrug‐resistant Enterococcus faecium, subsequent spread, and eventually infections. However, the events that occur at the initial stage of intestinal colonization and outgrowth by multidrug‐resistant E. faecium within the antibiotic‐treated host have not been thoroughly studied. Here, we describe and visualize that only 6 hr after cephalosporin treatment of mice, the Muc‐2 mucus layer is reduced and E‐cadherin junctions were altered. In contrast, the cadherin‐17 junctions were unaffected in antibiotic treated mice during E. faecium colonization or in untreated animals. E. faecium was capable to colonize the mouse colon already within 6 hr after inoculation, and agglutinated at the apical side of the intestinal epithelium. During the primary stage of gastrointestinal colonization the number of IgA(+) cells and CD11b(+)IgA(+) cells increased in the lamina propria of the colon and mediated an elevated IgA response upon E. faecium colonization. |
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