Epithelial regeneration in the bovine mammary gland: the clousre of lesions produced byEscherichia coli

Abstract

The repair of lesions in the bilayered non-secretory epithelium of the bovine mammary gland was studied in cases of experimental coliform mastitis by means of scanning and transmission electron microscopy. Lesions were produced in the lactiferous and teat sinuses of six quarters of three cows by infusing small numbers (250-700 colony-forming units) of a virulent strain ofEscherichia coli(B117). Glands were examined at intervals up to 30 h after infection. The earliest sign of lesion closure was observed in two quarters that had been infected for 15 h and 18 h respectively. The mounds of polymorphs that had accumulated over the lesions had dispersed to reveal a fibrin clot. Marginal cells of the basal epithelial layer became very flat, produced broad lamellipodia and started to migrate across the denuded basement membrane. These were followed by a succession of submarginal cells which usually moved as a sheet but were also capable of migrating independently. Some basal cells ingested small particles of extracellular material as they migrated under the fibrin clot. Marginal cells of the superficial epithelial layer behaved in two, quite different ways. In some areas they were flattened, produced prominent lamellipodia and migrated relative to the basal cells. Their submarginal cells showed no sign of active movement and were probably pulled along by the marginal cells. Most marginal cells, however, were inactive. In these cases, the submarginal cells were very active and produced long basal processes that underlapped the adjacent marginal cells. Cell migration proceeded while bacteria were still present in the vicinity of the lesion. Cells derived from the basal layer eventually formed a continuous monolayer covering the lesion but the re-formation of a complete superficial layer was not followed in this study. By comparing the progress of the disease in glands infected for different periods of time it was deduced that complete closure of lesions may take less than 5 h. The rapidity of closure and hence the restoration of the blood-milk barrier was attributed in part to the retention of an intact basement membrane during lesion formation. No increase in the incidence of mitotic figures was detected in the epithelia during the period of recovery studied.