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Infect Immun. 1980 Dec;30(3):718-22.

Depression of the respiratory burst in alveolar and peritoneal macrophages after thermal injury.


The resting O(2) consumption of alveolar and peritoneal macrophages obtained from rats at 4 and 24 h after thermal injury was unaltered from control values. However, when heat-killed Pseudomonas aeruginosa or polystyrene latex particles were added to the cell suspensions to initiate phagocytosis, a significant depression in the respiratory burst accompanying the phagocytic event was demonstrated. The addition of phorbol myristate acetate, used to maximize the respiratory response, was ineffective in elevating, to control values, the respiratory burst of macrophages obtained from burned animals. The deficit was only, in part, serum mediated since the responses could not be restored to control values even when the cells from the burned animals were vigorously washed with control serum and incubated with control serum. The contribution of a burn serum factor, which was non-dialyzable, heat stable at 56 degrees C but not at 65 degrees C, and insensitive to pronase treatment, must be considered. These data indicate that thermal injury results in macrophage metabolic alterations which are mediated, in part, by a burn serum factor. Furthermore, the data suggest that pulmonary alveolar macrophages are more sensitive to thermal injury than peritoneal macrophages. Serum factors contributed, in part, to this observed impairment in the respiratory burst as indicated by: (i) an approximate 50% reversal of the impairment by control serum, and (ii) an approximate decrease of 50 to 80% in the control alveolar macrophage respiratory burst when serum from the thermally injured rats was added to the culture medium.

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