Abstract
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.
| Original language | English |
|---|---|
| Article number | e00602 |
| Number of pages | 11 |
| Journal | MicrobiologyOpen |
| Volume | 7 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Oct 2018 |
Keywords
- CD11b IgA cells
- E-cadherin
- antibiotic-resistant E. faecium
- cadherin-17
- intestinal colonization
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