Mechanisms of Immunity in Typhus Infections IV. Failure of Chicken Embryo Cells in Culture to Restrict Growth of Antibody-Sensitized
            <i>Rickettsia prowazeki</i>

Wisseman, Charles L.; Waddell, Anna; Walsh, W. T.

doi:10.1128/iai.9.3.571-575.1974

Cited by 18 publications

(11 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is suggested that antibody-sensitized rickettsiae are capable of entering and replicating within the guinea pig's endothelial cells. This possibility is supported by the demonstration that antibodies which prepare R. prowazekii for destruction by macrophages (1,5) do not prevent this parasite from entering or replicating within chicken embryo cells (16), cells which are not professional phagocytes.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of immunity in typhus infection: adoptive transfer of immunity to Rickettsia mooseri

Murphy¹,

Wisseman²,

Fiset³

1979

Infect Immun

View full text Add to dashboard Cite

When nonimmune guinea pigs are inoculated intradermally (id.) with Rickettsia mooseri (R. typhi), the rickettsiae replicate at the site of inoculation, leading to the development of a grossly observable lesion. In contrast, guinea pigs which have recovered from R. mooseri infection are resistant to challenge and prevent both rickettsial growth and the formation of lesions. To study the mechanisms of this immunity, sera or splenic cells collected from nonimmune or immune guinea pigs were inoculated separately into nonimmune recipients. Splenic cells collected from immune donors protected R. mooseri-naive recipients from i.d. challenge as measured by control of rickettsial growth and by prevention of development of lesions at i.d. sites ofinoculation. In contrast, serum from immune and nonimmune donors failed to protect nonimmune recipients by either criterion.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanisms of immunity in typhus infection: adoptive transfer of immunity to Rickettsia mooseri

Murphy¹,

Wisseman²,

Fiset³

1979

Infect Immun

View full text Add to dashboard Cite

show abstract

“…These data, along with those of Cohn et al (5) and Wisseman et al (24,(26)(27)(28), allow the beginnings of a model of rickettsial invasion of host cells. Our results suggest that each native rickettsia adheres specifically to the target cell surface, where it triggers the host endocytic mechanism, and the adherent rickettsia is rapidly phagocytized.…”

Section: Walker and Winklermentioning

confidence: 53%

“…We have utilized a new, radioactive assay to characterize the invasion of L cells by R. prowazeki. This assay offers several advantages over the microscopic assays previously used (5,24,26,28) in studies on rickettsial invasiveness. Microscopic assessment of rickettsial invasion into cultured cells is tedious, requiring subjective examination of hundreds of individual host cells to insure reliability.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Penetration of Cultured Mouse Fibroblasts (L Cells) by Rickettsia prowazeki

1978

View full text Add to dashboard Cite

The association of Rickettsia prowazeki with L cells was examined by using a novel radioactive assay in which [a-32P]ATP-labeled rickettsiae were incubated with L-cell monolayers. Rickettsial association with the monolayer involved adherence and internalization steps that could be experimentally distinguished. Since R. prowazeki but not L cells possess an ATP-ADP obligate exchange transport system, addition of excess unlabeled ATP resulted in exchange of the labeled ATP from external, adherent rickettsiae but not from internalized rickettsiae. Rickettsial association was temperature dependent and was a linear function of both time and concentration. More than 90% of the biologically active rickettsiae associated with L cells was internalized. Rickettsial internalization required active participation of both rickettsiae and L cells; inactivation of either greatly reduced internalization. Rickettsial adherence to poisoned L cells was a saturable function of time and concentration. Adherence showed less temperature dependence than did internalization, but like rickettsial internalization, the extent of adherence was extremely low at 0°C. The rate and extent of adherence by inactivated and native rickettsiae to inactivated L cells were similar. Although inactive rickettsiae adhered to active and inactive L cells to a similar extent, inactive rickettsiae were internalized poorly by active L cells. These data form the basis for the hypothesis that R. prowazeki are internalized by the host cell through a process of "induced phagocytosis" and that inactivated rickettsiae adhere to the host cell differently from native rickettsiae, failing to trigger the endocytosis mechanism.

show abstract

“…However, the growth of virulent rickettsiae which have been treated with specific antisera prior to infection is inhibited in macrophage cells and macrophagelike cell lines (1,5,6,10). In contrast, specific antiserum-treated rickettsiae of either strain grow normally in fibroblasts (10,17), indicating that the combination of the antiserum and a macrophage-specific factor is necessary for antirickettsial activity. Macrophagelike cells are used since they are similar to human macrophages in their interaction with R. prowazekii, are clonal and subject to less heterogeneity, and undergo a respiratory burst and since a mutant cell line exists that has lost this ability.…”

mentioning

confidence: 99%

Roles of the Fc receptor and respiratory burst in killing of Rickettsia prowazekii by macrophagelike cell lines

1989

View full text Add to dashboard Cite

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-_4C]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.

show abstract

Mechanisms of Immunity in Typhus Infections IV. Failure of Chicken Embryo Cells in Culture to Restrict Growth of Antibody-Sensitized Rickettsia prowazeki

Cited by 18 publications

References 7 publications

Mechanisms of immunity in typhus infection: adoptive transfer of immunity to Rickettsia mooseri

Mechanisms of immunity in typhus infection: adoptive transfer of immunity to Rickettsia mooseri

Penetration of Cultured Mouse Fibroblasts (L Cells) by Rickettsia prowazeki

Roles of the Fc receptor and respiratory burst in killing of Rickettsia prowazekii by macrophagelike cell lines

Contact Info

Product

Resources

About