Influence of Thorotrast Blockade and Acute Renal Artery Ligation on Disapperance of Staphylococcal Enterotoxin B from Blood

Rapoport, Morton I.; Hodoval, Leland F.; Beisel, William R.

doi:10.1128/jb.93.3.779-783.1967

Cited by 18 publications

(5 citation statements)

References 13 publications

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“…labeled SEB, fluorescein-labeled anti-SEB immunoglobulin, or fluorescein-labeled SEB, in both in vitro and in vivo settings (6,7,22,(24)(25)(26)(27)(28). However, all of the studies employed the i.v.…”

mentioning

confidence: 99%

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Beery¹,

Taylor²,

Schlunz³

et al. 1984

Infect Immun

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Staphylococcal enterotoxin A (SEA) was administered orally (15 jig) to two groups of rats. A marked immune reaction was evoked in the stomach and proximal small intestine of the first group. The second group of rats was used to study the absorptive fate and sites of action of orally administered SEA, utilizing immunoperoxidase staining. After oral dosing of the second group of rats, SEA-related immunoperoxidase staining was confined to: (i) neutrophils and macrophages, principally in the duodenum, and (ii) glomerular neutrophils and cells of the proximal convoluted tubules. Peroxidase staining of the kidney was noted within 15 min of exposure, indicating that SEA or some major postabsorption antigenic product can promptly pass through an intact gastrointestinal mucous membrane and become renally localized. Intestinal and renal detoxification and removal was indicated by an absence of detectable antigen in rats 180 min postexposure. Neuronal binding of SEA in the gastrointestinal tract was not demonstrable.

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mentioning

confidence: 99%

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Beery¹,

Taylor²,

Schlunz³

et al. 1984

Infect Immun

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“…Evidence from experiments performed using animal models implicates the kidney in general, and the REPTCs in particular, as the major target of SEB uptake. It is also clear that 70% of injected SEB is accumulated in proximal tubule cells within 2 h [29–31] of stimulation. Based on the evidence of kidney involvement in blood pressure regulation, it is not unreasonable to hypothesize that damage to the renal epithelium caused by a vascular shock‐inducing agent, such as SEB (which possesses the ability to interact directly with the vascular tone‐regulating kidney cells), may contribute to the development of systemic shock (unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Effect of 5‐lipoxygenase inhibitor MK591 on early molecular and signaling events induced by staphylococcal enterotoxin B in human peripheral blood mononuclear cells

Mendis¹,

Campbell²,

Das³

et al. 2008

The FEBS Journal

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Staphylococcal enterotoxin B (SEB) is one of the many exotoxins produce by Staphylococcus aureus and is implicated in inducing diarrhea, vomiting, muscle numbness, possible involvement in autoimmune disorders and lethal shock [1]. The massive impact of T cell activation, proliferation, and cytokine production by CD4 + T cells via specific V b elements of T cell antigen receptor [2] has prompted a number of investigations to focus on the intricate signaling activities of SEB. Even though the molecular events of SEB-induced lethal shock in human peripheral blood mononuclear cell (PBMCs) are not very apparent, the actual response of lethal shock is expected to herald by changes in signaling pathways [3,4]. In mammalian cells, a variety of stimuli generate intracellular responses that converge on a limited number of components of multiple pathways [5]. Mitogen-activated protein kinase (MAPK) cascades together with arachidonic Staphylococcal enterotoxin B (SEB) has been the focus of a number of studies due to its ability to promote septic shock and a massive impact on the human immune system. Even though symptoms and pathology associated with SEB is well known, early molecular events that lead to lethality are still poorly understood. Our approach was to utilize SEB induced human peripheral blood mononuclear cells (PBMCs) as a prototype module to further investigate the complexity of signaling cascades that may ultimately lead to lethal shock. Our study revealed the activation of multiple divergent intracellular pathways within minutes of SEB induction including components that interconnect investigated pathways. A series of performed inhibi-tor studies identified a specific inhibitor of 5-LO (MK591), which has the ability to block JNK, MAPK, p38kinase and 5-LO signaling-cascades and drastically reducing the activity of pro-inflammatory cytokine TNF-a. Further evaluation of MK591 utilizing cell proliferation assays in PBMCs, human proximal tubule cells and in vivo studies (monkey) showed a decrease in cell proliferation. The inhibitory effect of MK591 was reconfirmed at a genetic level through the utilization of a set of SEB specific genes. Signaling activities, inhibitor studies, cellular analysis and gene expression analysis in unison illustrated the significance of pathway inter-connectors such as 5-LO as well as inhibiting such inter-connectors (using MK591) in SEB induced human PBMCs. Abbreviations 5-LO, 5-lipoxygenase; HIF, hypoxia-inducible factor; IL, interleukin; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; p38kinase, p38-mitogen activated protein kinase; PBMC, peripheral blood mononuclear cell; REPTC, renal epithelial proximal tubular cell; SEB, staphylococcal enterotoxin B; TNF, tumor necrosis factor.

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“…While similarities in the toxic manifestations of the endotoxin and the enterotoxin have been observed and both materials are rapidly cleared from the plasma of experimental animals, a difference has been found after blockade of the RES in monkeys. 328 With the use of highly purified enterotoxin B labeled with P31, it was found that effective blockade of the RES did not produce a significant change in the rapid disappearance kinetics of the enterotoxin. Acute bilateral renal artery ligation on the other hand produced a profound delay in enterotoxin clearance from the plasma.…”

Section: Clinical Pharmacology and Therapeuticsmentioning

confidence: 99%

The botulinal, tetanal, and enterostaphylococcal toxins: A review

Lamanna¹,

Cj²

1967

Clin Pharma and Therapeutics

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It is our wish to consider the current status of knowledge and to stimulate awareness of the problems and opportunities existing for future studies of the nature and actions of the botulinal, tetanal, and enterostaphylococcal toxins. Increasing knowledge makes such a review timely. In the light of the selective actions of botulinal and tetanal toxins on autonomic and central nervous system interneuronal mechanisms, it is remarkable that one finds no references to these very useful agents in the outstanding texts and reference volumes in neurophysiology and pharmacology. Successful methods of purification now make it possible to employ these toxins as specific reprodUCible and selective reagents or aids in the study of physioReceived for publication Oct. 5, 1966. 286logical and pharmacological questions, a potential that has not been exploited maximally.It is logical to consider these three exotoxins of gram positive bacteria in a single paper because in common they have been proven to be neurotoxic simple proteins. Our attention will not be focused on the purely bacteriological questions of the origin of these toxins in the bacterial economy and environmental factors influencing their production and occurrence in clinical illness. Nor will we consider the clinical problem of tetanus and botulism in medical and veterinary practice, and the occurrence of botulism in wildlife. Reviews including subject matter we have not covered are available. 90 , 93, 114, 115, 128, 135, 154, 156, 177,249,307,308 We will consider primarily the nature and actions of the toxins.

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Influence of Thorotrast Blockade and Acute Renal Artery Ligation on Disapperance of Staphylococcal Enterotoxin B from Blood

Cited by 18 publications

References 13 publications

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Effect of 5‐lipoxygenase inhibitor MK591 on early molecular and signaling events induced by staphylococcal enterotoxin B in human peripheral blood mononuclear cells

The botulinal, tetanal, and enterostaphylococcal toxins: A review

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