Meeting report Twelfth Midwinter Conference of Immunologists. January 6-9, 1973.
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Biomedical subjects
Publications and source records attributed to H H Fudenberg.
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The increased susceptibility to pyogenic infections noted in cattle with the Chediak-Higashi syndrome trait has been related to an impairment of leukocyte function at the cellular level. Investigations of the relationship of abnormal granule formation to increased susceptibility to infection, conducted with cell suspensions containing high concentrations of polymorphonuclear leukocytes, revealed a bactericidal defect that was associated with abnormal intracellular killing and not due to defective particle ingestion. The in vitro bactericidal defect was associated with a metabolic anomaly in the hexose monophosphate shunt, but not with an alteration in the capacity to reduce nitroblue tetrazolium dye. Ultrastructural histochemical studies of phagocytosis and phagolysosome formation in polymorphonuclear leukocytes suggest that the impairment in bactericidal capacity is correlated also with either a delay or failure of primary granules to degranulate.
In rat peritoneal macrophages, engaged in erythrophagocytosis in vitro, endotoxin stimulated heme oxygenase (HO) activity, which was additive to the substrate-mediated enzyme induction produced by the ingested erythrocyte hemoglobin. Endotoxin neither appeared to injure the erythrocytes, nor did it enhance the rate of erythrophagocytosis. In intact rats, HO activity in both parenchymal and sinusoidal cells of the liver was increased after treatment with endotoxin. It is likely that endotoxin directly stimulates HO activity, a process which may account for the reported rise in bilirubin formation in endotoxin-treated animals. The effect of endotoxin on HO may represent part of the general activation of phagocytic cells by endotoxin.
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