T cell control of staphylococcal enterotoxin B (SEB) lethal sensitivity in mice: CD4+ CD45RBbright / CD4+ CD45RBdim balance defines susceptibility to SEB toxicity

Canaan, Allon; Marcus, Hadar; Burakova, Tanya; David, M.M.; Dekel, Benjamin; Segall, Harry; Reisner, Yaīr

doi:10.1002/(sici)1521-4141(199904)29:04<1375::aid-immu1375>3.0.co;2-n

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…Hallmark studies during the 1990s showed that the toxicity of SEB was due to massive T-cell proliferation and proinflammatory cytokine production White et al, 1989). Investigations using T-cell reconstituted immuno-deficient SCID mice confirmed the role of T-cell activation in SE-induced lethality (Miethke et al, 1992;Canaan, et al 1999). Furthermore, these studies indicated that tumor necrosis factor alpha (TNF-) plays a crucial role in SE-induced lethality because passive immunization with an anti-TNF-/ monoclonal antibody protected the animals against an SE challenge (Fast et al, 1989;Miethke et al, 1992).…”

Section: Toxic Shock Syndromementioning

confidence: 98%

Staphylococcal Enterotoxins, Stayphylococcal Enterotoxin B and Bioterrorism

Hale¹

2012

Bioterrorism

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Section: Toxic Shock Syndromementioning

confidence: 98%

Staphylococcal Enterotoxins, Stayphylococcal Enterotoxin B and Bioterrorism

Hale¹

2012

Bioterrorism

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Trypanosoma Cruzi Sensitizes Mice to Fulminant Seb-Induced Shock: Overrelease of Inflammatory Cytokines and Independence of Chagas' Disease or TCR V??-Usage

Paiva

Pyrrho²,

Lannes-Vieira³

et al. 2003

Shock

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Trypanosoma cruzi-infected mice display increased susceptibility to shock induced by injection of lipopolysaccharide (LPS), anti-CD3, or resulting from interleukin (IL)-10-defective response to the parasite itself, but the basis of such susceptibility remains unknown. Herein, we tested the susceptibility of mice inoculated with virulent and avirulent T. cruzi to staphylococcal enterotoxins (SE), potent inducers of inflammatory cytokine secretion. Mice infected with T. cruzi CL-strain or inoculated with the avirulent clone CL-14, a clone that does not induce disease or polyclonal lymphocyte activation, succumb suddenly to low doses of staphylococcal enterotoxin B (SEB), but not to staphylococcal enterotoxin A (SEA). High plasma levels of TNF, IFN-gamma, and liver transaminases alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were found in these mice, indicating lethal toxic shock. Sensitization to shock required inoculation of live avirulent trypomastigotes and a time interval before challenge with SEB. We found no prior skewing of T cell receptor (TCR) Vbeta-repertoire in CL-14-inoculated mice that could be responsible for sensitization. Splenocytes from CL-14-inoculated mice proliferated more under anti-Vbeta8 than anti-TCRbeta stimulation when compared with normal mice, but were suppressed to SEB stimulation. Both SEB and anti-Vbeta8 antibodies stimulated splenocytes from T. cruzi-inoculated mice to secrete higher levels of inflammatory cytokines than normal controls. Taken together, our results show that T. cruzi inoculation can sensitize mice to lethal SEB-induced shock even in the absence of tissue damage, polyclonal lymphocyte activation, or previously increased levels of inflammatory cytokines, and they suggest that altered reactivity of Vbeta8 lymphocytes may be involved in the phenomenon.

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Tumour suppression induced by the macrophage activating lipopeptide MALP-2 in an ultrasound guided pancreatic carcinoma mouse model

Schneider

Schmidt²,

Ziske³

et al. 2004

Gut

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Background and aim: Carcinoma of the exocrine pancreas has a particularly poor prognosis. Therefore, novel therapeutic strategies such as immunotherapy are required. Here we investigated the immunomodulatory capacity of macrophage activating lipopeptide 2 (MALP-2), which binds to toll-like receptors 2 and 6 and induces activation of nuclear factor kB in monocytes. This causes the release of early stage leucocyte attracting chemokines and proinflammatory cytokines. Methods: MALP-2 was tested in a new orthotopic ultrasound guided pancreatic cancer mouse model. This model is close to the biological situation and avoids the stress and immunostimulation caused by laparotomy. Cells from the syngeneic, highly aggressive, and metastatic cell line Panc 02 were administered orthotopically, by ultrasound guidance, to C57bl/6 mice. MALP-2 was administered intratumorally or intraperitoneally and tumour growth, immune status, and leucocyte infiltration at the tumour site were determined. Results: We showed a tumour suppressive effect induced by a single injection of MALP-2. Median survival increased from 21 to 30 days (p,0.002). Combining chemotherapy (gemcitabine) with MALP-2 treatment caused further prolonged survival (median survival 27 days with chemotherapy alone v 37 days for combined treatment; p,0.0002). The life prolonging effect was paralleled by a significant increase in cytotoxic T cells, restoration of b2 integrin expression on lymphocytes, and high expression of CD45RB on T helper cells. Immunohistochemical stains showed strong cytotoxic T lymphocyte and natural killer cell infiltration. Conclusions: In conclusion, in a model of orthotopic pancreatic cancer in mice, we induced a tumour suppressive effect by treatment with a synthetic lipopeptide. Treatment with MALP-2 could be an option for immunotherapy in pancreatic cancer.

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T cell control of staphylococcal enterotoxin B (SEB) lethal sensitivity in mice: CD4+ CD45RBbright / CD4+ CD45RBdim balance defines susceptibility to SEB toxicity

Cited by 3 publications

References 21 publications

Staphylococcal Enterotoxins, Stayphylococcal Enterotoxin B and Bioterrorism

Staphylococcal Enterotoxins, Stayphylococcal Enterotoxin B and Bioterrorism

Trypanosoma Cruzi Sensitizes Mice to Fulminant Seb-Induced Shock: Overrelease of Inflammatory Cytokines and Independence of Chagas' Disease or TCR V??-Usage

Tumour suppression induced by the macrophage activating lipopeptide MALP-2 in an ultrasound guided pancreatic carcinoma mouse model

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