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Research Article Free access | 10.1172/JCI107788

Pulmonary Alveolar Macrophage DEFENDER AGAINST BACTERIAL INFECTION OF THE LUNG

Elliot Goldstein, William Lippert, and David Warshauer

1Section of Infectious and Immunologic Diseases, Department of Internal Medicine, School of Medicine, University of California, Davis, California 95616

Find articles by Goldstein, E. in: JCI | PubMed | Google Scholar

1Section of Infectious and Immunologic Diseases, Department of Internal Medicine, School of Medicine, University of California, Davis, California 95616

Find articles by Lippert, W. in: JCI | PubMed | Google Scholar

1Section of Infectious and Immunologic Diseases, Department of Internal Medicine, School of Medicine, University of California, Davis, California 95616

Find articles by Warshauer, D. in: JCI | PubMed | Google Scholar

Published September 1, 1974 - More info

Published in Volume 54, Issue 3 on September 1, 1974
J Clin Invest. 1974;54(3):519–528. https://doi.org/10.1172/JCI107788.
© 1974 The American Society for Clinical Investigation
Published September 1, 1974 - Version history
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Abstract

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, 2½, 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 2½ and 5 h were 44.5% and 76.9%, respectively. The percentages of intracellular bacteria were: 0 h, 54.8%; 2½ 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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