Roles of the Fc receptor and respiratory burst in killing of Rickettsia prowazekii by macrophagelike cell lines.
It is known that the virulent strain of Rickettsia prowazekii grows in macrophagelike cell lines, but if the rickettsiae are treated with antirickettsial serum before infection, the intracellular rickettsiae fail to grow and are destroyed. The uptake of rickettsiae by macrophagelike cell lines was increased by treatment of the rickettsiae with immune serum and with purified immunoglobulin G (IgG) from this serum but not by treatment with the F(ab')2 fragment derived from this IgG. This suggested that the normal rickettsial pathway of entry could be augmented by the Fc receptor-mediated pathway. However, rickettsiae treated with these F(ab')2 fragments which contained no Fc region were destroyed as effectively as those treated with immune serum or IgG. Internalization of R. prowazekii (whether virulent, avirulent, treated, or untreated) did not lead to an increased release of CO2 from [1-14C]glucose, an increase that would have been indicative of a respiratory burst. Furthermore, a mutant macrophagelike cell line, incapable of a respiratory burst, was able to destroy rickettsiae treated with immune serum as effectively as did the parental cell line. Electron micrographs of macrophagelike cells which had been incubated with either antirickettsial IgG or with F(ab')2 fragments derived from this IgG both demonstrated marked deterioration of the rickettsiae, which were primarily within vacuoles but occasionally free in the cytoplasm. In contrast, untreated rickettsiae displayed morphologically normal rickettsiae which were mostly in the cytoplasm but occasionally in the intact and damaged vacuoles. These results indicated that (i) a respiratory burst was not a significant part of the mechanism used by macrophagelike cells to destroy R. prowazekii treated with immune serum, (ii) the destruction of the rickettsiae by the macrophage was not dependent on a diversion to the Fc receptor-mediated pathway of entry, and (iii) the locus of damage to the rickettsiae was most likely the phagolysosome of the macrophagelike cell line.
Keysary
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Department of Microbiology and Immunology, University of South Alabama College of Medicine, Mobile 36688.
McCaul
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TF
Winkler
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D000818:Animals; D002460:Cell Line; D007106:Immune Sera / Q000494:pharmacology; D007140:Immunoglobulin Fab Fragments / Q000502:physiology; D007074:Immunoglobulin G / Q000502:physiology; D008264:Macrophages / Q000276:immunology / Q000382:microbiology / Q000502:physiology*; D051379:Mice; D008854:Microscopy, Electron; D010101:Oxygen Consumption; D010427:Pentose Phosphate Pathway; D011961:Receptors, Fc / Q000502:physiology*; D012283:Rickettsia prowazekii / Q000254:growth & development* / Q000276:immunology / Q000648:ultrastructure
D007106:Immune Sera; D007140:Immunoglobulin Fab Fragments; D007074:Immunoglobulin G; D011961:Receptors, Fc