Suppression of cellular immune responses in guinea pigs infected with spotted fever group rickettsiae

Oster, Charles N.; Kenyon, Richard H.; Pedersen, Carl E.

doi:10.1128/iai.22.2.411-417.1978

Cited by 7 publications

(6 citation statements)

References 19 publications

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“…There was no evidence of suppression of lymphocyte transformation to mitogens by vaccination nor was suppression of lymphocyte transformation to mitogens observed after challenge of these animals. This is in contrast to the report of Oster et al (10) who reported a transient depression of lymphocyte responses within a few days after infection with R. rickettsii. It is possible that we did not observe the decreased lymphocyte responses because we were studying lymphocyte transformation 28 days after challenge, and the depressed responses noted by Oster et al (10) were seen in the first 10 days after infection.…”

Section: Discussioncontrasting

confidence: 99%

“…This is in contrast to the report of Oster et al (10) who reported a transient depression of lymphocyte responses within a few days after infection with R. rickettsii. It is possible that we did not observe the decreased lymphocyte responses because we were studying lymphocyte transformation 28 days after challenge, and the depressed responses noted by Oster et al (10) were seen in the first 10 days after infection. No immunopathological sequelae of vaccination or postvaccination challenge were observed in these experiments, and no systemic toxicity of the vaccine was noted.…”

Section: Discussioncontrasting

confidence: 99%

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Rocky Mountain spotted fever vaccine in an animal model

Folds¹,

Walker²,

Hegarty³

et al. 1983

J Clin Microbiol

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Formalin-killed, purified Rickettsia rickettsii vaccine was evaluated in a guinea pig model of R. rickettsii infection. Vaccinated guinea pigs were partially protected by the vaccine when challenged with virulent, viable rickettsiae. Greater protection was observed when higher doses of vaccine were given and when frequent booster injections were administered. Stimulation of cell-mediated immunity to the vaccine antigens was variable and also appeared to be achieved more reproducibly with booster vaccinations. Serum antibody was elicited by high doses of vaccine and by booster vaccinations. The presence of serum antibody was useful in predicting immunity to challenge with R. rickettsii. Rocky Mountain spotted fever (RMSF) is an acute febrile illness caused by Rickettsia rickettsii. The disease has a significant mortality rate and is a disease for which a vaccine is needed to protect individuals living in endemic areas. The vaccines which were available previously have not reliably prevented infection by R. rickettsii (2, 13). Previous vaccines consisted of killed R. rickettsii harvested either from infected ticks (13) or from embryonated hen eggs (2). Both vaccines contained nonrickettsial antigens of eggs or whole macerated ticks and offered incomplete protection against disease. The purpose of this investigation was to evaluate a Formalin-inactivated R. rickettsii vaccine Sheila Smith strain (SS strain), chick embryo cell culture origin (freeze-dried lot no. 1), supplied by the United States Army Medical Research Institute of Infectious Diseases (USAM-RIID), Frederick, Md. (5) in a guinea pig model. Infection of guinea pigs with R. rickettsii gives a

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 99%

Rocky Mountain spotted fever vaccine in an animal model

Folds¹,

Walker²,

Hegarty³

et al. 1983

J Clin Microbiol

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“…Infection of experimental animals with spotted fever group rickettsiae has been shown to lead to a suppression of cellular immune response that extends to both rickettsial and unrelated antigens (19). It is possible that the development of antigen-specific suppressor cells influenced the in vitro responses in this study.…”

Section: Resultsmentioning

confidence: 86%

“…The presence of cellular immunity in human and experimental animals convalescent from spotted fever group rickettsial infections has been suggested on the basis of well-established in vitro parameters of cell-mediated immunity, including lymphocyte prolif-* Corresponding author. eration in response to specific antigenic stimulation (3,11,19). The necessity of T cells in resistance to spotted fever group rickettsiae was also suggested by the studies of Kenyon and Pedersen (12) on congenitally athymic (nulnu) mice infected with R. akari.…”

mentioning

confidence: 96%

Cross-reactive lymphocyte responses and protective immunity against other spotted fever group rickettsiae in mice immunized with Rickettsia conorii

Jerrells¹,

Jarboe²,

Eisemann³

1986

Infect Immun

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Lymphocyte proliferation in response to antigens on spotted fever group rickettsiae was used as a method to investigate the group-specific protective immunity to rechallenge characteristic of this group of rickettsiae at the T-cell receptor level. Spleen cells from Rickettsia conorii-immune C3H/HeJ mice proliferated in response to R. rickettsii Sheila Smith, R. sibirica 246, R. australis, and all tested strains of R. conorii (Casablanca, Moroccan, and Malish). Spleen cells from these mice, however, responded poorly or not at all to antigens prepared from the Kaplan or Hartford strain ofR. akari. Proliferation of immune T cells maintained as in vitro cell lines showed a similar pattern of reactivity to these antigens; however, response to R. akari was consistently demonstrable. Spleen cells from C3H/HeJ mice immunized with R. akari responded to R. akari and R. conorii antigens as well as antigens from the other spotted fever group rickettsiae. Lymphocytes obtained from lymph nodes draining foot pads infected with R. conorii or R. akari demonstrated cross-reactivity similar to that found with immune spleen cells. If immunization was accomplished with R. conorii antigen emulsified in Freund complete adjuvant, the resulting lymph node cells were able to respond to R. akari antigens. These data suggest that infection with R. conorii induces a population of T lymphocytes that recognize an antigen(s) that also is found on other spotted fever rickettsiae and that may be responsible for cross-protective immunity. This antigen probably is not a major antigen on R. akari.

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“…Even among other rickettsiae, the duration of the immunosuppressive response to C. burnetii is unusually lengthy. Oster et al (31) observed that suppression of lymphocyte proliferation in guinea pigs infected with Rickettsia ricketsii subsided by day 17; Rickettsia sibirica and Rickettsia conorii caused suppression of lymphocyte proliferation only through day 7. In the present study, the persistence of the hyporesponsive condition may result from an ineffectual clearance of the antigen from tissues by the host.…”

Section: Discussionmentioning

confidence: 99%

Suppression of in vitro lymphocyte proliferation in C57BL/10 ScN mice vaccinated with phase I Coxiella burnetii

Damrow¹,

Williams²,

Waag³

1985

Infect Immun

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The effect of inactivated phase I and phase II Coxiella burnetii whole cell vaccine (WCV) on the response of murine spleen cells to mitogenic and antigenic stimuli was evaluated in C57BL/10 ScN endotoxin nonresponder mice with an in vitro lymphocyte proliferation assay. Intraperitoneal injection of phase I WCV into mice resulted in marked and persistent suppression of the proliferative response of spleen cells to concanavalin A, phytohemagglutinin, and pokeweed mitogen. This response was time and dose dependent and was not associated with decreased lymphocyte viability. By using a standard dose of 100 ,ug of phase I WCV, suppression of mitogenic responsiveness was first detected 3 days postinjection, attained maximum levels by day 14, and persisted for longer than 5 weeks. Suppression of mitogenic lymphocyte proliferation also was demonstrated after inoculation of animals with viable phase I organisms. The observed hyporesponsiveness of spleen cells from phase I WCV-injected animals was not either the result of a shift in the mitogenic dose optimum or due to a change in the day of in vitro peak response. Spleen cells from phase I WCV-injected mice were negatively regulated with homologous antigen. Investigation of the mechanism of action of phase I WCV, with a 51Cr-release assay, and trypan blue dye exclusion showed that phase I WCV was not directly cytolytic or cytotoxic to spleen cells from normal or vaccinated mice. Phase II WCV did not induce significant mitogenic hyporesponsiveness or negative modulation of spleen cells. These findings extend the observations of adverse host responses associated with the phase I WCV and underscore the need to develop a microbial fraction which possesses protective potency but which lacks the immunosuppression.propensity to induce deleterious tissue reactions and Vaccination against Q fever in humans was introduced in 1948 by Smadel et al. (39). The whole cell vaccine (WCV) consisted of a formalin-inactivated suspension of Coxiella burnetii prepared from infected yolk sacs. The protective value of phase I WCV has been well documented (19,28,30,43). Despite the prophylactic efficacy of phase I WCV, we are concerned about the potential for adverse reactions induced by phase I WCV (45). When phase I WCV was first developed and tested, Smadel et al. observed local skin reactions, fever, anorexia, and malaise in vaccinated individuals (39). Since then, various severe local reactions (28) and occasional systemic reactions (45) have been described. Recently, phase I WCV administered intraperitoneally has been shown to induce splenomegaly, hepatomegaly, liver necrosis, and anemia in C57BL/10 ScN mice (45). The undesirable effects of phase I WCV have been severe enough to preclude its widespread and unconditional use in humans (1).The effect of the phase I C. burnetii WCV in mice has been defined largely in terms of gross pathological changes. In a previous study, the subject of host cellular immunological functions was broached and the occurrence of mitogenic hyporesponsiveness in C5...

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Suppression of cellular immune responses in guinea pigs infected with spotted fever group rickettsiae

Cited by 7 publications

References 19 publications

Rocky Mountain spotted fever vaccine in an animal model

Rocky Mountain spotted fever vaccine in an animal model

Cross-reactive lymphocyte responses and protective immunity against other spotted fever group rickettsiae in mice immunized with Rickettsia conorii

Suppression of in vitro lymphocyte proliferation in C57BL/10 ScN mice vaccinated with phase I Coxiella burnetii

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