Patterns of Interferon-γ mRNA Expression in Toxic Shock Syndrome Toxin-1 Expanded Vβ11+ T Lymphocytes

Zhao, Yi‐Xue; Abdelnour, Arturo; Ljungdahl, Å.; Olsson, Tomas; Tarkowski, Andrej

doi:10.1006/cimm.1995.1005

Cited by 26 publications

(23 citation statements)

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“…In addition, the decreased number of class II-expressing cells due to lack of the B-cell population might have affected the superantigenic responses, since the IFN-␥ is a cytokine whose secretion is readily triggered by TSST-1 (22). Finally, it has recently been shown that clonal expansion of superantigen-reactive T cells is diminished in MT mice compared to intact controls (20).…”

Section: Discussionmentioning

confidence: 99%

Are B Lymphocytes of Importance in SevereStaphylococcus aureusInfections?

et al. 2000

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To investigate the role of B cells in experimental, superantigen-mediated Staphylococcus aureus arthritis and sepsis, we used gene-targeted B-cell-deficient mice. The mice were inoculated intravenously with a toxic shock syndrome toxin 1 (TSST-1)-producing S. aureus strain. The B-cell-deficient and thus agamma-globulinemic mice showed striking similarities to the wild-type control animals with respect to the development of arthritis, the mortality rate, and the rate of bacterial clearance. Surprisingly, we found that the levels of gamma interferon in serum were significantly lower (P < 0.0001) in B-cell-deficient mice than in the controls, possibly due to impaired superantigen presentation and a diminished expression of costimulatory molecules. In contrast, the levels of interleukin-4 (IL-4), IL-6, and IL-10 in serum were equal in both groups. Our findings demonstrate that neither mature B cells nor their products significantly contribute to the course of S. aureus-induced septic arthritis.We have previously described a murine model of hematogenously induced Staphylococcus aureus arthritis and sepsis (7,8). Using this model, approximately 80 to 90% of mice inoculated with S. aureus LS-1 develop clinical arthritis. Immunohistochemical analysis of arthritic joints demonstrated the presence of phagocytes and T cells, predominantly of the CD4 phenotype (4). The infected mice displayed increased levels of inflammatory cytokines, such as tumor necrosis factor and interleukin-6 (IL-6) in serum (7). We have also shown that toxic shock syndrome toxin 1 (TSST-1), a superantigen produced by S. aureus LS-1, contributes to the arthritogenicity of S. aureus (3,5). A series of studies using this model suggested that S. aureus arthritis is a T-cell-dependent and superantigen mediated disease.As to the role of B cells in S. aureus arthritis, we have found that a striking feature in this model is the occurrence of polyclonal B-cell activation with highly increased levels of immunoglobulins and autoantibodies in serum (7). Using X-linked immunodeficiency (xid) mice to investigate the contribution of the B1 subset of B cells to the development of septic arthritis, it was found that this defect provided resistance (21). Since the B1 subset is considered to be of importance in the production of autoantibodies, it was hypothesized that the outcome of the experiment might have been due to this fact.The aim of this study was to investigate if mature B cells, irrespective of their B1 or B2 phenotype, and their products including cytokines, autoantibodies, and antibodies to bacterial constituents would affect the outcome of S. aureus-induced arthritis and sepsis. We report here that a complete absence of mature B cells has no impact on the outcome of these very severe and life-threatening conditions. MATERIALS AND METHODSMice. Gene-targeted B-cell-deficient MT mice (C57BL/6 ϫ 129) (11) were backcrossed to B10.Q (H-2 q ) mice for eight generations and then further intercrossed for two generations to provide homozygous B10.Q mice lacking fu...

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Section: Discussionmentioning

confidence: 99%

Are B Lymphocytes of Importance in SevereStaphylococcus aureusInfections?

et al. 2000

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“…Splenocytes from uninfected and infected mice were prepared as previously described (53). Briefly, mouse spleens were passed through a nylon mesh and erythrocytes were depleted by hypotonic lysis.…”

Section: Mice Breeding Pairs Of Homozygous Tnfrp55mentioning

confidence: 99%

Tumor Necrosis Factor Receptor p55-Deficient Mice Respond to AcuteYersinia enterocoliticaInfection with Less Apoptosis and More Effective Host Resistance

et al. 2000

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Tumor necrosis factor (TNF) has generally been regarded as a protective cytokine in host defense against bacterial infections. In the present study, we evaluated the role of TNF in the acute phase of infection by Yersinia enterocolitica by using mice rendered genetically deficient in TNF receptor p55 (TNFRp55؊/؊ mice showed more effective resistance to the bacteria, reflected in enhanced bacterial clearance and less tissue damage, than did control C57BL/6 mice. C57BL/6 mice showed evidence of extensive apoptosis in the spleen accompanied by a selective decrease in the CD4 ؉ -T-cell population of splenocytes, whereas TNFRp55 ؊/؊ mice were spared these changes. The splenocytes from TNFRp55 ؊/؊ mice also maintained a robust gamma interferon IFN-␥ response to mitogenic stimulation, while the comparable response in C57BL/6 mice was impaired. In addition, splenocytes harvested from infected mice demonstrated lower production of interleukin-10 IL-10 in TNFRp55؊/؊ mice than in C57BL/6 mice. These findings suggest that Yersinia can induce TNFRp55-mediated apoptosis of splenocytes in the acute phase of the infection and that alteration of T-cell-generated cytokines can dramatically alter the early events in host defense against this pathogen.

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“…The enzyme substrate was then added, and the absorbance was measured in a Titertek Multiscan photometer (Flow Labs) at 405 nm. The samples were tested in two-fold dilutions and compared with recombinant mouse IFN-g standard (Genzyme) [29].…”

Section: Serological Analysismentioning

confidence: 99%

Complement depletion aggravatesStaphylococcus aureussepticaemia and septic arthritis

Sakiniene

Bremell

Tarkowski

1999

Clinical and Experimental Immunology

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SUMMARYThe aim of the study was to assess the role of the complement system in Staphylococcus aureus arthritis and septicaemia. The murine model of haematogenously acquired septic arthritis was used, injecting intravenously toxic shock syndrome toxin-1 (TSST-1), producing S. aureus LS-1. Complement was depleted using cobra venom factor (CVF). Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of complement depletion on the phagocytic activity of leucocytes was assessed in vivo and in vitro. Six days after inoculation of S. aureus the prevalence of arthritis in decomplemented mice was three-fold higher than that in controls (91% versus 25%). The clinical severity of arthritis at the end of the experiment, expressed as arthritic index, was 7·3 and 1·9, respectively. These findings were confirmed by histological index of synovitis as well as of cartilage and/or bone destruction being significantly higher in decomplemented mice than in controls (9·8 Ϯ 1·7 versus 4·9 Ϯ 1·2, P < 0·05; and 7·9 Ϯ 1·7 versus 3·0 Ϯ 0·9, P < 0·05, respectively). Also, the septicaemiainduced mortality was clearly higher in decomplemented mice compared with the controls. CVF treatment significantly reduced in vivo polymorphonuclear cell-dependent inflammation induced by subcutaneous injection of olive oil and mirroring the capacity of polymorphonuclear cells (PMNC) to migrate and/or extravasate. Besides, the decomplementation procedure significantly impaired phagocytic activity of peripheral blood leucocytes in vitro, since the number of phagocytes being able to ingest bacteria decreased by 50% when the cells were maintained in decomplemented serum compared with those in intact serum. The conclusion is that complement depletion aggravates the clinical course of S. aureus arthritis and septicaemia, possibly by a combination of decreased migration/extravasation of PMNC and an impairment of phagocytosis.

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Patterns of Interferon-γ mRNA Expression in Toxic Shock Syndrome Toxin-1 Expanded Vβ11+ T Lymphocytes

Cited by 26 publications

References 0 publications

Are B Lymphocytes of Importance in SevereStaphylococcus aureusInfections?

Are B Lymphocytes of Importance in SevereStaphylococcus aureusInfections?

Tumor Necrosis Factor Receptor p55-Deficient Mice Respond to AcuteYersinia enterocoliticaInfection with Less Apoptosis and More Effective Host Resistance

Complement depletion aggravatesStaphylococcus aureussepticaemia and septic arthritis

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