Suppression of the in Vivo Humoral and Cellular Immune Response by Staphylococcal Enterotoxin B (Seb)

Pinto, Mary Beth; Torten, M.; Birnbaum, S.

doi:10.1097/00007890-197806000-00008

Cited by 48 publications

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“…The potencies of staphylococcal SAgs differ with toxin type and the origin of the cells used in the proliferation assay, but generally concentrations as low as 0.1 to 100 ng/ml have mitogenic effects (3,45). In addition to causing proliferation of T cells and an uncontrolled release of cytokines like tumor necrosis factor alpha, interleukin-2, and IFN-␥ (45), SAgs can induce populations of suppressor cells and reduce humoral immune responses (7,34). In the present study, the rise in IFN-␥ production with increasing SED concentrations corresponded with the findings in the lymphocyte proliferation assay.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Enterotoxin D Is Secreted in Milk and Stimulates Specific Antibody Responses in Cows in the Course of Experimental Intramammary Infection

2006

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An enterotoxin D (SED)-producing strain of Staphylococcus aureus was used to infect one mammary gland of each of 17 lactating dairy cows. All glands became infected and shed bacteria over a sampling period of 3 weeks. Serum and milk antibodies specific for SED were monitored by an enzyme-linked immunosorbent assay for 12 weeks. Elevated anti-SED antibodies were detected in all cows after infection, and immunoglobulin of the G2 subclass comprised most of the specific serum response. SED was detected in mastitic milk samples from two cows at levels of 5 to 10 ng/ml. An in vitro lymphocyte proliferation assay showed that SED at levels below 10 pg/ml induced proliferation of bovine lymphocytes and that sheep antiserum specific for SED neutralized this proliferative response. Sera obtained from the cows pre-and postinfection inhibited lymphocyte proliferation at SED concentrations of 10 and 50 ng/ml, respectively. The addition of SED to whole blood or to isolated neutrophils had no significant effect on neutrophil function in vitro. The results show that SED is secreted during mammary gland infection, is mitogenic for bovine lymphocytes, and stimulates the production of specific antibodies.Staphylococcus aureus is a major cause of intramammary infection in ruminants and is a causative agent of a range of human and animal diseases. S. aureus mastitis tends to commence with an acute clinical episode which subsequently develops to become a chronic infection (1). The cure rate after antibiotic therapy is low (42). The chronic nature of bovine staphylococcal mastitis and the ability of the bacteria to withstand strong inflammatory responses may be associated with an impairment of the immune response mediated by factors secreted by S. aureus (39).S. aureus produces a family of related superantigens (SAgs) that includes several staphylococcal enterotoxins (SE) and toxicshock-syndrome toxin (TSST) variants (6). Staphylococcal SAgs are prototypical microbial superantigens, characterized by their ability to bind to major histocompatibility complex class II molecules and specific V␤ segments of ␣␤ T-cell receptors (32). SAgs bypass the antigenic specificities of T-cell receptors and stimulate abnormally large numbers of T cells. At extremely low concentrations, these molecules can induce profound disturbances in the homeostasis of the immune system (17, 44). These toxins play a critical role in human toxic shock syndrome and food poisoning, but their possible role in the onsets or maintenance of other diseases is not well understood (41).Geographical differences exist in the occurrence of SAg-producing strains causing mastitis (22). Kenny et al. (19) found that S. aureus strains producing enterotoxin D (SED) alone or in combination with S. aureus enterotoxin C (SEC) and TSST-1 accounted for 22% of the isolates from New York State. In Norway, a previous study showed that 58% of S. aureus isolates expressed SAgs and that the production of SEC and TSST-1 in combination predominated (40). Some reports have suggested that S. aureus...

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Enterotoxin D Is Secreted in Milk and Stimulates Specific Antibody Responses in Cows in the Course of Experimental Intramammary Infection

2006

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“…Although the data demonstrate that V~8 + CD4-CD8-expansion in lymphoid tissues is dramatically prevented in mice, the mechanisms whereby this therapy downregulates autoan-tibody and immune complex production are currently unclear. Previous data have demonstrated that SEB injection can cause suppression in the humoral response in normal mice (31), and thus it is possible that SEB can suppress anti-DNA antibody-producing B cells in MRL/Ipr mice.…”

Section: Discussionmentioning

confidence: 99%

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

Kim

Siminovitch

Ochi

1991

The Journal of Experimental Medicine

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Sllnlmal'yThe effects of biweekly intravenous injections of Staphylococcus Enterotoxin B (SEB) into autoimmune MRL, Ipr/lpr (MRL/Ipr) mice were investigated. Rather than causing the expansion of VB8 + T cells, SEB administration resulted in the reduction of VB8 +, CD4-CDS-"doublenegative" (DN) T cells. This was shown by FACS | analysis as this putative pathogenic population was diminished in both spleen and lymph node. The symptoms of systemic lupus erythematosus (SLE) in MRL/Ipr, which include high titers of anti-DNA antibodies and circulating immune complexes and proteinuria, were reduced in SEB-treated mice in a dose-dependent manner. The clinical parameters of SLE in MRL/~, which include lymph node hyperplasia and necrotic vasculitis, were suppressed in 50-#g SEB-treated mice. T cells bearing V~6 T cell receptor, which does not interact with SEB, were not reduced with SEB administration. Thus, disease suppression was associated with a specific reduction in the number of V~8 +, DN T cells. These results implicate a possible therapeutic role of superantigen-based immunotherapy in V~/-restricted, T cell-dominated clinical syndromes.S uperantigens (SuperAgs) 1 are molecules that in association with class II MHC activate T cells based solely on the V~ chain of the TCK (1, 2). These antigens are the most powerful polyclonal mitogens known, stimulating a large proportion of both murine and human T cells. The minor lymphocyte stimulating (Mls) antigen, a self-SuperAg, has recently been reported to be encoded by a retrovirus, but the Mls antigen has yet to be isolated (3-7). More is known about the bacterial Super_Ags, particularly the Staphylococcus aureus enterotoxin series (SEs), whose sequence and structure have been documented (1). SuperAgs are known to exert powerful effects on the developing TCR repertoire in both CD4 § and CD8 + T cells (8-11). Previous data from this laboratory (12, 13) and others (14) Abbreviations used in thispatx,

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“…It also has been reported that treatment with SEB in vivo results in suppression of both the humoral and cellular immune responses (40,41) as well as anergy of V,98' cells (42,43). Factors that may explain why SEB potentiates the antitumor response in our system while suppressing the immune response in other systems include differences in mouse strains, kinetics, route of administration, and perhaps differences in the antigens examined.…”

mentioning

confidence: 91%

In vivo T-cell activation by staphylococcal enterotoxin B prevents outgrowth of a malignant tumor.

Newell

Ellenhorn

Bruce

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Treatment of T cells with staphylococcal enterotoxns in vitro is known to activate T cells in a subset restricted manner based on fi-chain variable region (Vp) gene expression. In particular, staphylococcal enterotoxin B (SEB) activates T cells bearing Vp7 or Vp8. We examined the ability of SEB to activate T cells in vivo. Treatment of C3H mice with doses of SEB ranging from 5 to 250 Fg resulted in a dosedependent activation of Vp8' T cells as reflected by increased interleukin 2 receptor (IL-2R) expression, proliferation to exogenous IL-2 and aflogeneic cells, and production of y interferon. SEB also caused proliferation ofthe CD8+ subset of Vp8+ cells in vivo. Thus, T-cell activation by SEB in vivo appears to be specific since Vp2+ cells (non-SEB reactive) did not show increases in IL-2R expression similar to those seen with Vp8+ cells nor did they proliferate. We then studied the ability of these activated cells to potentiate the immune response to a malignant progressor tumor. Treatment of C3H mice with 50 jug of SEB at the time of inoculation with tumor fragments resulted in a statistically sigicant decrease in the frequency of tumor outgrowth. These data demonstrate that treatment of C3H mice with SEB results in specific activation of Vp8+ cells in vivo and that these activated cells are capable of preventing the outgrowth of a malignant tumor.

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Suppression of the in Vivo Humoral and Cellular Immune Response by Staphylococcal Enterotoxin B (Seb)

Cited by 48 publications

References 0 publications

Staphylococcus aureus Enterotoxin D Is Secreted in Milk and Stimulates Specific Antibody Responses in Cows in the Course of Experimental Intramammary Infection

Staphylococcus aureus Enterotoxin D Is Secreted in Milk and Stimulates Specific Antibody Responses in Cows in the Course of Experimental Intramammary Infection

Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment.

In vivo T-cell activation by staphylococcal enterotoxin B prevents outgrowth of a malignant tumor.

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