Abstract

We describe an experimental model of pneumonia in Wistar rats evoked by Streptococcus sanguis. The lesion developed rapidly as a confluent bronchopneumonia of the single-lobed left lung. Except at the extreme base, where an abscess formed, the pneumonic process thereafter resolved, and most of the lung appeared microscopically and ultrastructurally normal 8 days after infection. Sequential electron microscopic studies revealed that in the areas of lung which subsequently resolved, damage was restricted to type 1 pneumocytes. Within 24 h of infection, the unaffected type 2 pneumocytes were observed to proliferate, transform into elongated pneumocytes of intermediate morphology, and then undermine and strip off the damaged type 1 cells from the subjacent basement membrane. Thereafter, the intermediate type pneumocytes completed their transformation into definitive type 1 cells, thus completing the repair process. We hypothesize that this represents an accelerated form of the normal type 1 replacement mechanism, and that uncomplicated epithelial repair following acute alveolar damage is possible if type 2 pneumocytes escape significant damage, so that they retain their capacity to proliferate and differentiate into type 1 epithelium.

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