Pulmonary alveolar macrophage defender against bacterial infection of the lung

E Goldstein, W Lippert… - The Journal of clinical …, 1974 - Am Soc Clin Investig
E Goldstein, W Lippert, D Warshauer
The Journal of clinical investigation, 1974Am Soc Clin Investig
The rate of ingestion of inhaled bacteria by pulmonary alveolar macrophages is an important
determinant of host defense. This parameter was investigated by infecting rats with finely
dispersed aerosols bearing Staphylococcus aureus in high concentrations (about 10s
bacteria/ft3/min). These aerosols deposited more than 106 bacteria/murine lung. At 0, 2˝,
and 5 h after infection, bacterial clearance rates were measured in the left lung, and the
intracellular or extracellular location of 100 bacteria was determined histologically in the …
The rate of ingestion of inhaled bacteria by pulmonary alveolar macrophages is an important determinant of host defense. This parameter was investigated by infecting rats with finely dispersed aerosols bearing Staphylococcus aureus in high concentrations (about 10s bacteria/ft3/min). These aerosols deposited more than 106 bacteria/murine lung. At 0, 2˝, and 5 h after infection, bacterial clearance rates were measured in the left lung, and the intracellular or extracellular location of 100 bacteria was determined histologically in the right lung (perfused in situ). The clearance rates at 2˝ and 5 h were 44.5% and 76.9%, respectively. The percentages of intracellular bacteria were: 0 h, 54.8%; 2˝ h, 87.1%: 5 h, 91.9%. When rats were exposed for 4 h to 2.5 ppm of ozone (O3), bacterial clearance did not occur — 15.3%, although 78.7% of the bacteria were intracellular. Clumps of more than 10 bacteria—usually intracellular—were also present. These experiments demonstrate that phagocytic ingestion is an exceedingly rapid process, that in this experimental model the inactivation of inhaled staphylococci results almost entirely from phagocytosis, and that ozone-induced reductions in bacterial clearance are due to severe impairment of intrapulmonary killing mechanisms and minor impairment of bacterial ingestion.
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The Journal of Clinical Investigation