TY - JOUR
T1 - Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus infected murine lungs
AU - Jakab, G. J.
AU - Green, G. M.
PY - 1976
Y1 - 1976
N2 - Bacterial multiplication associated with virus infections is related to defects in in situ bactericidal (phagocytic) mechanisms of the lung. To determine whether the phagocytic defect was in bacterial ingestion and/or intracellular digestion, mice were infected with a sublethal dose of aerosolized Sendai virus and challenged 7 days later with a finely dispersed aerosol of Staphylococcus aureus. Groups of uninfected and virus infected mice were sacrificed at 0, 6, 12, and 24 hr after challenge, the lungs were perfused with formalin in situ, and the intra or extracellular location of the bacteria was determined histologically. At 0 h, 49% and 51% of the staphylococci had an intracellular location in virus and nonvirus infected lungs, respectively. With time, decreasing numbers of staphylococci were observed within the phagocytic cells of nonvirus infected lungs, mostly as single organisms or in small clusters of less than 4. In contrast, in foci of virus infected lungs, increasing numbers of phagocytic cells showed clumps of more than 25 bacteria/cell. These data demonstrate that virus infected suppression of pulmonary antibacterial activity against S. aureus is related primarily to defects in intracellular processing mechanisms.
AB - Bacterial multiplication associated with virus infections is related to defects in in situ bactericidal (phagocytic) mechanisms of the lung. To determine whether the phagocytic defect was in bacterial ingestion and/or intracellular digestion, mice were infected with a sublethal dose of aerosolized Sendai virus and challenged 7 days later with a finely dispersed aerosol of Staphylococcus aureus. Groups of uninfected and virus infected mice were sacrificed at 0, 6, 12, and 24 hr after challenge, the lungs were perfused with formalin in situ, and the intra or extracellular location of the bacteria was determined histologically. At 0 h, 49% and 51% of the staphylococci had an intracellular location in virus and nonvirus infected lungs, respectively. With time, decreasing numbers of staphylococci were observed within the phagocytic cells of nonvirus infected lungs, mostly as single organisms or in small clusters of less than 4. In contrast, in foci of virus infected lungs, increasing numbers of phagocytic cells showed clumps of more than 25 bacteria/cell. These data demonstrate that virus infected suppression of pulmonary antibacterial activity against S. aureus is related primarily to defects in intracellular processing mechanisms.
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U2 - 10.1172/JCI108423
DO - 10.1172/JCI108423
M3 - Article
C2 - 180054
AN - SCOPUS:0017072368
SN - 0021-9738
VL - 57
SP - 1533
EP - 1539
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 6
ER -