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. 1974 Sep;54(3):519-28.
doi: 10.1172/JCI107788.

Pulmonary alveolar macrophage. Defender against bacterial infection of the lung

Pulmonary alveolar macrophage. Defender against bacterial infection of the lung

E Goldstein et al. J Clin Invest. 1974 Sep.

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 10(s) bacteria/ft(3)/min). These aerosols deposited more than 10(6) bacteria/murine lung. At 0, 2(1/2), 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(1/2) and 5 h were 44.5% and 76.9%, respectively. The percentages of intracellular bacteria were: 0 h, 54.8%; 2(1/2) h, 87.1%: 5 h, 91.9%. When rats were exposed for 4 h to 2.5 ppm of ozone (O(3)), 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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References

    1. J Exp Med. 1968 Nov 1;128(5):1201-21 - PubMed
    1. J Appl Physiol. 1968 Jul;25(1):63-9 - PubMed
    1. Nature. 1971 Jan 22;229(5282):262-3 - PubMed
    1. Annu Rev Med. 1968;19:315-36 - PubMed
    1. J Theor Biol. 1968 Oct;21(1):103-12 - PubMed