Abstract
Summary A systematic study of the effect of acute radiation injury upon the natural resistance of mice to experimental pneumococcal myositis has revealed that the principal factor involved in the lowered resistance of the irradiated host is a marked depression in the mobilization of phagocytic cells at the site of the primary lesion. The delayed and diminished inflammatory response, which coincides with the postirradiation leukopenia, permits the pneumococci to reach a population density in the lesion approximately a thousand times greater than that observed in unirradiated mice. The relatively few leukocytes, which in these circumstances manage to reach the lesion, exhibit no demonstrable impairment of phagocytic activity and show only an equivocal change in their capacity to kill the pneumococci which they ingest.
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