Enhancement of Bacterial Endotoxin Lethality by Staphylococcal Enterotoxin

Sugiyama, Hiroki; McKissic, E. M.; Bergdoll, Merlin S.; Heller, Bárbara

doi:10.1093/infdis/114.2.111

Cited by 88 publications

(58 citation statements)

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“…The values represent the mean ϩ SD for duplicate samples from three experiments. Numerous investigations show that LPS potentiates the biologic effects of SEs and that septic shock may reflect a culmination of excessive proinflammatory cytokines resulting from the actions of both toxins (3,4,24,35,39,40,42). Although SE and LPS often lead to different sequelae, acute shock caused by abnormally high levels of TNF-␣ and other proinflammatory cytokines results in life-threatening situations (8,11,38).…”

Section: Fig 2 Levels Of Tnf-␣ (A) Ifn-␥ (B) Il-1␣ (C)mentioning

confidence: 99%

Pirfenidone Blocks the In Vitro and In Vivo Effects of Staphylococcal Enterotoxin B

Hale

Margolin²,

Krakauer

et al. 2002

Infect Immun

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Pirfenidone [5-methyl-1-phenyl-2-(1H)-pyridone] down-regulates expression of cytokines and other mediators involved in the onset and development of pulmonary fibrosis. Pirfenidone also inhibits production of tumor necrosis factor alpha (TNF-␣) from macrophages incubated with endotoxin and protects mice against endotoxin shock. Pirfenidone's ability to reduce cytokine expression in these disorders led us to investigate the drug's effect on another cytokine anomaly, superantigen-induced shock. BALB/c mice were exposed to staphylococcal enterotoxin B (SEB) either systemically or by aerosol and subsequently potentiated with a sublethal dose of lipopolysaccharide. In these experiments, pirfenidone given 2 to 4.25 h after SEB resulted in 80 to 100% survival versus only 0 to 10% survival among untreated control animals. Relative to serum cytokine levels from controls given toxin but no drug, there was a 35 to 80% decrease in TNF-␣, interleukin 1, and other proinflammatory cytokines. In vitro experiments with human peripheral blood lymphocytes revealed that pirfenidone reduced SEB-induced cytokine levels 50 to 80% and inhibited 95% of SEB-induced T-cell proliferation. Overall, these studies demonstrated the potential utility of pirfenidone as a therapeutic against septic shock and the biological effects of SEB.

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Section: Fig 2 Levels Of Tnf-␣ (A) Ifn-␥ (B) Il-1␣ (C)mentioning

confidence: 99%

Pirfenidone Blocks the In Vitro and In Vivo Effects of Staphylococcal Enterotoxin B

Hale

Margolin²,

Krakauer

et al. 2002

Infect Immun

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“…Rabbits have been used in staphylococcal toxin research including staphylococcal enterotoxins even before their superantigenicity was established. 27 However, even the rabbit model of TSS seems to require sensitization with lipopolysaccharide to induce death, 28,29 or require continuous infusion of SAg for 7 days. 30 Moreover, even in the rabbit model of TSS, extensive investigation of the temporal changes in systemic cytokine and chemokine concentrations, an indepth immunopathologic characterization of multiple-organ disease, and ultimately the correlation between systemic inflammatory response, multiple-organ disease, and the outcome of TSS have not been performed.…”

mentioning

confidence: 99%

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Tilahun

Marietta

et al. 2011

The American Journal of Pathology

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Among the exotoxins produced by Staphylococcus aureus and Streptococcus pyogenes, the superantigens (SAgs) are the most potent T-cell activators known to date. SAgs are implicated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis. However, the immunopathogenesis of TSS and other diseases involving SAgs are still not completely understood. The commonly used conventional laboratory mouse strains do not respond robustly to SAgs in vivo. Therefore, they must be artificially rendered susceptible to TSS by using sensitizing agents such as D-galactosamine (D-galN), which skews the disease exclusively to the liver and, hence, is not representative of the disease in humans. SAg-induced TSS was characterized using transgenic mice expressing HLA class II molecules that are extremely susceptible to TSS without D-galN. HLA-DR3 transgenic mice recapitulated TSS in humans with extensive multiple-organ inflammation affecting the lung, liver, kidneys, heart, and small intestines. Heavy infiltration with T lymphocytes (both CD4 ؉ and CD8؉), neutrophils, and macrophages was noted. In particular, the pathologic changes in the small intestines were extensive and accompanied by significantly altered absorptive functions of the enterocytes. In contrast to massive liver failure alone in the D-galN sensitization model of TSS, findings of the present study suggest that gut dysfunction might be a key pathogenic event that leads to high morbidity and mortality in humans with

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“…(These experiments are not included fomsgram-negeacter have stmlae considerable research for two decades (4)(5)(6). in figure 2 because no deaths occurred at 4' C.…”

Section: I11 Results Charide Obtained From Salmonella Cnteritidismentioning

confidence: 99%

Influence of Temperature on the Effects of Enterotoxin and Endotoxin in Mice

Glenn¹

1970

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Enhancement of Bacterial Endotoxin Lethality by Staphylococcal Enterotoxin

Cited by 88 publications

References 0 publications

Pirfenidone Blocks the In Vitro and In Vivo Effects of Staphylococcal Enterotoxin B

Pirfenidone Blocks the In Vitro and In Vivo Effects of Staphylococcal Enterotoxin B

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Influence of Temperature on the Effects of Enterotoxin and Endotoxin in Mice

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