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The ultrastructure of transmissible murine colonic hyperplasia
Abstract:
Transmissible murine colonic hyperplasia was examined ultrastructurally by sequential sampling after inoculation with the etiologic agent, Citobacter freundii. Light-microscopic changes in the descending colon of inoculated mice were correlated with scanning and transmission electron-microsopic findings. Bacteria were attached to the surface of the mucosa between 4 and 10 days after inoculation. Hyperplasia was most severe at 16 days and thereafter underwent regression. Regression was preceded by extrusion of infected cells from the surface mucosa and replacement by immature hyperplasia epithelium. Hyperplastic epithelium throughtout the crypt resembled undifferentiated crypt cells of controls. By 45 days, the mucosa had reverted to near normal structure. The results suggest that severe mucosal proliferation with minimal inflammatory change resulted from attachment of bacteria to the surface mucosal epithelium. The hyperplastic response appeared to be a defense mechanism of replacing infected cells with newly migrated, uninfected epithelium.
Insights
This study reveals that Citrobacter freundii attachment to mouse colonic mucosa triggers hyperplasia. This epithelial proliferation appears to be a defense mechanism, with near-normal structure returning by 45 days.
Area of Science:
- Microbiology
- Gastroenterology
- Pathology
Background:
- Transmissible murine colonic hyperplasia is a condition affecting the colon of mice.
- Citrobacter freundii has been identified as the etiologic agent responsible for this condition.
Purpose of the Study:
- To ultrastructurally examine the development and regression of transmissible murine colonic hyperplasia.
- To correlate light microscopic changes with scanning and transmission electron microscopic findings.
Main Methods:
- Sequential sampling of the descending colon in inoculated mice.
- Light microscopy, scanning electron microscopy, and transmission electron microscopy were employed.
- Inoculation with the etiologic agent, Citrobacter freundii.
Main Results:
- Bacteria attached to the mucosal surface between 4 and 10 days post-inoculation.
- Maximal hyperplasia occurred at 16 days, followed by regression.
- Regression involved extrusion of infected cells and replacement by immature hyperplastic epithelium, which resembled undifferentiated crypt cells.
Conclusions:
- Severe mucosal proliferation resulted from bacterial attachment to the surface epithelium with minimal inflammation.
- The hyperplastic response is suggested to be a host defense mechanism.
- The colonic mucosa reverted to near-normal structure by 45 days post-inoculation.