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PubMed1982

Enterotoxin production at 4 degrees, 22 degrees, and 37 degrees C and Y. enterocolitica-like bacteria.

Production of heat-stable enterotoxin after cultivation at 4 degrees C for four days was indicated for 27 of 171 Yersinia enterocolitica and Y. enterocolitica-like bacteria, using the infant mouse assay. Of these 27 strains, 11 showed enterotoxin production at both 4 degrees and 22 degrees C, and the remaining 16 strains at 4 degrees, 22 degrees, and 37 degrees C. No strain was enterotoxigenic at 4 degrees C only. The relative prevalence of enterotoxin production at 4 degrees, 22 degrees, and 37 degrees C among Y. enterocolitica and Y. enterocolitica-like bacteria is presented. The results indicate that Y. kristensenii has a unique standing with respect to enterotoxigenicity at 4 degrees and at 37 degrees C. Y. kristensenii showed the highest prevalence of enterotoxin production at 4 degrees C (47%) and at 37 degrees C(49%). These properties were also recorded among environmental isolates of Y. enterocolitica sensu stricto, but the prevalences were low (4 and 1 %, respectively). The strains producing enterotoxin at 4 degrees C were different from those associated with yersiniosis and belonged to serogroups frequently isolated from small mammals, water, and soil (0:1, 6, 11, 12, 16, 28, and non-agglutinable). It is possible that such strains may contaminate foods and provoke food-borne intoxication involving pre-formed enterotoxins.

Animals↗

PubMed1992

Mechanism of action of a cytotonic enterotoxin produced by Aeromonas hydrophila.

In this study, we describe the mechanism of action of a cytotonic enterotoxin produced by two isolates of Aeromonas hydrophila. Isolates SSU and Ah65 are of different origin and both are capable of producing either a cytotoxic enterotoxin or aerolysin. A cytotonic enterotoxin produced by diarrheal isolate SSU, which was purified and characterized in our laboratory, elevated intracellular cAMP and PgE2 levels in cultured Chinese hamster ovary (CHO) cells. Likewise, enterotoxic activity expressed by a cytotonic enterotoxin was detected in the culture filtrate of a fish isolate (Ah65) after cytotoxic activity was neutralized with homologous aerolysin monoclonal antibodies. This cytotonic enterotoxin also elevated intracellular cAMP and PgE2 levels in CHO cells, suggesting a cholera toxin-like mechanism of action for Aeromonas cytotonic enterotoxins.

Aeromonas hydrophila↗

PubMedDate not supplied

Review of selected bacterial enterotoxins and their role in gastroenteritis.

The study of enterotoxins began in earnest approximately 30 years ago with characterization of the cholera toxin. So far, more enterotoxins have been associated with Gram-negative rather than Gram-positive bacteria. These substances can be roughly divided into the cytotonic variety, which primarily interfere with intestinal cell metabolism, and those which are cytotoxic, responsible for cell destruction. Most cytotonic enterotoxins activate cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) producing watery diarrhea, resulting from fluid and electrolyte flux. This typically results after binding to a toxin-specific receptor site on the small intestinal epithelium. Cytotoxic enterotoxins may interfere with protein synthesis in cells of the colonic epithelium and cause bloody, sometimes fatal dysentery. As more enterotoxins are discovered, it is becoming apparent that such variables as anatomic site and mode of action may not, in fact, be definitive criteria for classifying these substances. As a result, no universally acceptable classification scheme has yet been devised. Moreover, the biochemical and physiological characteristics of many enterotoxins and their role in gastroenteritis and other disorders remain speculative.

Endotoxins↗

PubMed2003

Bacterial enterotoxins are associated with resistance to colon cancer.

One half million patients suffer from colorectal cancer in industrialized nations, yet this disease exhibits a low incidence in under-developed countries. This geographic imbalance suggests an environmental contribution to the resistance of endemic populations to intestinal neoplasia. A common epidemiological characteristic of these colon cancer-spared regions is the prevalence of enterotoxigenic bacteria associated with diarrheal disease. Here, a bacterial heat-stable enterotoxin was demonstrated to suppress colon cancer cell proliferation by a guanylyl cyclase C-mediated signaling cascade. The heat-stable enterotoxin suppressed proliferation by increasing intracellular cGMP, an effect mimicked by the cell-permeant analog 8-br-cGMP. The antiproliferative effects of the enterotoxin and 8-br-cGMP were reversed by L-cis-diltiazem, a cyclic nucleotide-gated channel inhibitor, as well as by removal of extracellular Ca(2+), or chelation of intracellular Ca(2+). In fact, both the enterotoxin and 8-br-cGMP induced an L-cis-diltiazem-sensitive conductance, promoting Ca(2+) influx and inhibition of DNA synthesis in colon cancer cells. Induction of this previously unrecognized antiproliferative signaling pathway by bacterial enterotoxin could contribute to the resistance of endemic populations to intestinal neoplasia, and offers a paradigm for targeted prevention and therapy of primary and metastatic colorectal cancer.

Bacterial Toxins↗

PubMed1994

Characterization and partial purification of the human receptor for the heat-stable enterotoxin.

The receptor for the Escherichia coli heat-stable enterotoxin has been characterized and partially purified from the T84 human colonic cell line. Using a novel mutant heat-stable enterotoxin peptide as a radioligand (the C-terminal tyrosine residue is replaced by phenylalanine in the mutant), a single class of high-affinity receptor sites was detected in T84 cells, with a Kd of 0.1 nM, similar in affinity to the receptor described in human intestinal tissue. The receptor was solubilised from T84 cell membranes and affinity cross-linking of the solubilised preparation indicated that a single species of M(r) 160,000 served as the receptor. Freshly solubilised preparations of the receptor retained heat-stable enterotoxin-activable guanylyl cyclase activity. Purification of the receptor was achieved through sequential affinity chromatography on GTP--epoxy-Sepharose and wheat-germ-agglutinin columns resulting in purification of the receptor by 3000 fold. The heat-stable enterotoxin-binding characteristics of the receptor were unchanged during the purification and silver staining of the purified receptor preparation indicated a band of M(r) 160,000, which was specifically cross-linked to the 125I-labeled mutant peptide. The purified receptor retained guanylyl cyclase activity, but the activity was not stimulated on addition of human heat-stable enterotoxin, suggesting that accessory structural factors may be involved in the activation of the guanylyl cyclase/receptor.

Bacterial Toxins↗

PubMed2005

Interruption of homologous desensitization in cyclic guanosine 3',5'-monophosphate signaling restores colon cancer cytostasis by bacterial enterotoxins.

Bacterial diarrheagenic heat-stable enterotoxins induce colon cancer cell cytostasis by targeting guanylyl cyclase C (GCC) signaling. Anticancer actions of these toxins are mediated by cyclic guanosine 3',5'-monophosphate (cGMP)-dependent influx of Ca2+ through cyclic nucleotide-gated channels. However, prolonged stimulation of GCC produces resistance in tumor cells to heat-stable enterotoxin-induced cytostasis. Resistance reflects rapid (tachyphylaxis) and slow (bradyphylaxis) mechanisms of desensitization induced by cGMP. Tachyphylaxis is mediated by cGMP-dependent protein kinase, which limits the conductance of cyclic nucleotide-gated channels, reducing the influx of Ca2+ propagating the antiproliferative signal from the membrane to the nucleus. In contrast, bradyphylaxis is mediated by cGMP-dependent allosteric activation of phosphodiesterase 5, which shapes the amplitude and duration of heat-stable enterotoxin-dependent cyclic nucleotide accumulation required for cytostasis. Importantly, interruption of tachyphylaxis and bradyphylaxis restores cancer cell cytostasis induced by heat-stable enterotoxins. Thus, regimens that incorporate cytostatic bacterial enterotoxins and inhibitors of cGMP-mediated desensitization offer a previously unrecognized therapeutic paradigm for treatment and prevention of colorectal cancer.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1992

Gangliosides inhibit serological reactions for the detection of cholera and heat-labile enterotoxins of Escherichia coli.

GM1 ganglioside has been identified as the receptor for cholera toxin (CT) and heat-labile (LT) enterotoxin of Escherichia coli in many cell types. Using the radial immune hemolysis (RIH) and indirect hemagglutination (IH) tests described for the detection of these enterotoxins, a study was conducted on the 100% inhibition of these reactions by pre-incubating these enterotoxins with GM1, GD1a and GT1 gangliosides. GM1 was found to be much more efficient than the other two. With respect to the RIH test, GT1 was more efficient than GD1a as an inhibitor of enterotoxin binding. Similar results were obtained with the IH test. These data also showed that sheep red blood cells provide a good model system for the study of receptors for CT, LT and probably other enterotoxins which bind to gangliosides.

Animals↗

PubMed1995

Modification of immediate hypersensitivity responses by staphylococcal enterotoxin B.

The staphylococcal enterotoxins have been termed superantigens based on their ability to stimulate polyclonal proliferative responses of murine and human T lymphocytes expressing particular T-cell receptor V beta gene products. Certain of these toxins have been shown both to activate and to induce anergy in reactive T cells. Staphylococcal enterotoxin B is known to interact with murine T cells bearing V beta 3, -7, -8.1, -8.2, -8.3, and -17. In BALB/c mice V beta 3+ and V beta 17+ T cells are deleted; V beta 7+ T cells are low in frequency. BALB/c mice sensitized to ovalbumin via the skin and airways develop immediate hypersensitivity including IgE/IgG1 antiovalbumin antibodies, immediate cutaneous reactivity to ovalbumin and, increased airway responsiveness. In both in vitro and in vivo studies, the development of these responses has been associated with the V beta 8+ subset of T cells and controlled by V beta 2 + T cells. In view of the central role of V beta 8+ T cells in these responses, we tested the effects of staphylococcal enterotoxin B on the development of immediate hypersensitivity in this system. Intradermal injection of staphylococcal enterotoxin B prevented the development of these responses in the absence of a major deletion of V beta 8+ T cells. The data suggest that the administration of staphylococcal enterotoxin B prevented the antigen-induced expansion of V beta 8+ T cells resulting in a state of responsiveness or anergy, thus preventing the manifestations of immediate hypersensitivity. Bacterial toxins may provide a novel approach to intervention in allergic or autoimmune diseases.

Allergens↗

PubMed1977

The effect of attapulgite and charcoal on enterotoxicity of Vibrio cholerae and Escherichia coli enterotoxins in rabbits.

Vibrio cholerae and certain strains of Escherichia coli produce heat-labile enterotoxins which play a significant role in the pathogenesis of the intestinal disease. Activated attapulgite, a heated magnesium aluminum silicate, was previously shown to prevent the toxic effects of endotoxin. The present study has revealed that this drug inhibits the toxic effects of cholera and E. coli enterotoxins in the intestinal loop of rabbits, when toxin and attapulgite are pre-incubated prior to injection. Up to 50 to 100 minimal effective doses are inhibited. Attapulgite is effective also when injected separately, albeit simultaneously, into the intestinal loops, but not when administered after the toxin. Since supernates of toxinattapulgite mixtures are non-toxic, it is postulated that attapulgite acts by adsorption and that the attached enterotoxin is no longer toxic to the rabbit intestine. The previously reported effect of charcoal on V. cholerae enterotoxin paralleling that of attapulgite, was confirmed. In contrast to the effects of these absorbents on isolated toxin, both failed to prevent enterotoxicity in the rabbit model of an enterotoxin-producing strain of E. coli.

Aluminum Silicates↗

PubMed1975

Scanning isoelectric focusing of cholera enterotoxin in polyacrylamide gels.

Scanning isoelectric focusing has been employed for continuous monitoring of the isoelectric spectrum of highly purified cholera enterotoxin in 4% polyacrylamide gels containing 2% ampholytes pH 3-10. The resolution obtained by this technique is of high order because at no instance during focusing interruption of current occurs and thus diffusion of the isolated protein moieties is suppressed. An added aspect of scanning isoelectric focusing was that it allowed estimation of the minimal focusing time of cholera enterotoxin. Thus under the standard assay procedure, the main basic component of cholera enterotoxin was focused in 5800 sec, while the other at least 3 minor acidic and anodic components were focused in approximately 19000 sec. Focusing of cholera enterotoxin in the presence of 6 mu urea allowed the visualization of 5 well defined and about equal components. The proteinaceous nature of the observed peaks was verified by scanning at wavelenghts other than 280 nm, staining of gels for protein, and varying the concentration of the enterotoxin. The design of scanning isoelectric focusing equipment is presented. Reproducibility, economy of sample, and ampholytes and simplicity of experimental technique were some of the features of this apparatus. The resolution of scanning isoelectric focusing was found to be superior to that of ordinary disc and SDS gel electrophoresis.

Acrylamides↗

PubMed2006

Anaerobic cells of Bacillus cereus F4430/73 respond to low oxidoreduction potential by metabolic readjustments and activation of enterotoxin expression.

In the present study, a food-borne pathogen strain of Bacillus cereus (F4430/73) was anaerobically grown in controlled-batch conditions under low initial oxidoreduction potential (ORP=-148 mV) using hydrogen gas as reducing agent. Its physiological characteristics, including growth, glucose fermentation capacity and enterotoxin production, were compared with anaerobic conditions generated by nitrogen gas (ORP=+ 45 mV). The results showed that low ORP affected growth mainly during the early stages. Maximal specific rates of growth and glucose consumption were reduced, and drastic changes in time profiles of fermentation product concentration were observed. Production of lactate was promoted at the expense of acetate. Nevertheless, low ORP did not affect final biomass yield. Under both ORP conditions, Non-haemolytic enterotoxin (Nhe) was produced early during the exponential growth phase as a first enterotoxin and Haemolysin BL (Hbl) later during the early stationary growth phase as a second enterotoxin. The major effect of low ORP was the strong stimulation of Hbl production and, to a lesser extent, Nhe production. This control was complex, involving different levels of regulation. We discussed the regulation of enterotoxin expression and the involvement of the pleiotropic regulator PlcR.

Anaerobiosis↗

PubMed1981

Trypsin activation of enterotoxin from Clostridium perfringens type A: fragmentation and some physicochemical properties.

Clostridium perfringens type A enterotoxin was activated about 3-fold by treatment with trypsin, without an observed change in molecular weight. On denaturation in 8 M urea, the trypsinated enterotoxin lost a small peptide of about 4000 daltons. The single cysteine residue of enterotoxin was in the small peptide together with seven out of nine residues of proline. Trypsin activation, without removal of the small peptide, increased the 'outside' number of amino groups from eight to eleven. The trypsin treatment of the enterotoxin did not change the antigenic properties of the protein. Glycine was the C-terminal residue of the native enterotoxin while the dansyl alpha-amino acid of the N-terminal could not be identified.

Amino Acids↗

PubMed1992

Direct activation of murine T cells by staphylococcal enterotoxins.

The capacity of staphylococcal enterotoxins to stimulate all T cells bearing certain TCR variable region alleles has generated a great deal of interest. This stimulation appears to involve specific binding of the toxin to class II molecules and subsequent stimulation of the T cell via the TCR V beta elements. Recent studies from our laboratory have focused on the ability of staphylococcal enterotoxins to directly activate purified lymph node T cells and a panel of T cell clones and hybridomas. A T cell costimulation assay was performed to assess cellular activation requirements and cytokine receptor expression. Activation of highly purified lymph node T cells by staphylococcal enterotoxin B (SEB) required costimulatory signals which could be provided by IL-1, IL-2, IL-4, or IL-6, whereas SEB alone demonstrated no significant proliferative response. Using a panel of TH1 and TH2 cell clones and T cell hybridomas possessing various responsive and nonresponsive V beta alleles, it was possible to demonstrate that SEA and SEB costimulate T cells via the TCR complex. Additionally, enterotoxin-pretreated T cells demonstrated a significant proliferative response upon exposure to class II-bearing accessory cells, suggesting that these toxins bind directly to T cells. Highly purified T cells cultured with both SEB and IL-1 exhibit significantly increased levels of IL-2 receptor, whereas cells cultured with SEB or IL-1 alone demonstrated low levels of this receptor. These results do not exclude an association of the staphylococcal enterotoxins with class II molecules in a manner which results in a high avidity binding to the TCR required for transduction of the appropriate activation signals. In the absence of class II molecules, however, these superantigens can still bind to T cells, and the activation signal is delivered in the presence of cytokines that trigger T cell growth and lymphokine production.

Animals↗

PubMed1989

Development of a fluorescent immunodot assay for Bacillus cereus enterotoxin.

A fluorescent immunodot assay has been developed for rapid, specific detection of B. cereus enterotoxin. None of the other Bacillus species tested showed cross-reactivity in the assay with antiserum to purified B. cereus enterotoxin. The assay can detect greater than or equal to 50 ng of purified enterotoxin. Using this assay system, enterotoxin was found to be produced by 25 of 25 foodborne disease-related isolates and 22 of 25 isolates not related to foodborne disease (isolates from routine surveillance foods). Because of the apparent widespread ability of isolates to produce enterotoxin the assay may have potential as a rapid identification procedure for B. cereus. The substrate gel system described may have wider application in other immunoassay systems using a membrane solid phase.

Bacillus cereus↗

PubMed1990

Temperature limits of growth, TNase and enterotoxin production of Staphylococcus aureus strains isolated from foods.

For 77 strains of Staphylococcus aureus freshly isolated from different foods, growth, enterotoxin and TNase production were determined in intervals of 1.5 degrees C +/- 0.5 degrees C by cultivating them in a temperature-gradient incubator between 5 and 50 degrees C for up to 7 days. All the strains were coagulase, DNase and lysostaphin positive but only 58% formed one or two enterotoxins type SEA, SEB or SEE. All strains grew within 7 days in brain heart infusion and had lower and upper temperature limits for growth and TNase production of between 6.5 and 12.5 degrees C, and 39.5 and 48.5 degrees C respectively. The lower and upper temperature limits for production of enterotoxins were between 14 and 38 degrees C, and between 35 and 44 degrees C respectively. Enterotoxin forming isolates either showed narrow (3 to 4 degrees C) or wide (10 to 20 degrees C) ranges of enterotoxin production, irrespective of their temperature range of growth and TNase production. None of the 12 specific physiological attributes used for differentiation could be correlated to toxin type or the temperature requirement of the toxin production. No correlation between the origin and the physiological characters could be detected.

Enterotoxins↗

PubMed1990

Production and properties of crude enterotoxin of Pseudomonas aeruginosa.

Pseudomonas aeruginosa CTM-3 was found to be the most potentially enterotoxigenic strain out of the 12 isolates recovered from milk, as a high fluid length ratio, i.e. F/L (1.1) in rabbit gut and a strong permeability response in rabbit skin (38.5 mm2 necrotic zone) was obtained with this culture. No clear-cut relationship between the two tests was observed. Six of the ethidium bromide (300 micrograms/ml) cured variants of this culture completely lost their ability to produce enterotoxin indicating the possible involvement of a plasmid in enterotoxin synthesis. The crude enterotoxin from P. aeruginosa CTM-3 was completely inactivated in 15 s at 72 degrees C. However, it was fairly stable at pH values in the range 4.5-7.5. Both pepsin and trypsin inactivated the enterotoxin activity at a concentration of 40 micrograms/ml. Organic acids, formalin and hydrogen peroxide had no significant effect on the enterotoxin activity. The need for further investigations with purified preparations is emphasized.

Animals↗

PubMed1996

Enterotoxin production by coagulase-negative staphylococci isolated from goats' milk and cheese.

An antigen related to the Enterotoxin E from Staphylococcus aureus was produced by ten of 187 coagulase-negative staphylococci (CNS) isolated from goats' milk, whey and cheese in quantities ranging from 10 to 90 ng/ml supernatant. The enterotoxin-producing strains were identified at the species level as S. simulans, S. xylosus, S. equorum, S. lentus and S. capitis. Detection of the enterotoxins was done by the VIDAS SET test (bioMérieux) and by an indirect double-sandwich ELISA technique using anti-enterotoxin monoclonal antibodies. The results obtained were further confirmed by Southern blotting, using two radioactive oligonucleotide probes that hybridized specifically with the gene of S. aureus coding for the enterotoxin E.

Animals↗

PubMed1980

Mode of action of heat-stable Escherichia coli enterotoxin. Tissue and subcellular specificities and role of cyclic GMP.

Some enteric strains of Escherichia coli release a heat-stable enterotoxin which, in contrast to cholera and heat-labile E. coli enterotoxins, stimulates guanylate cyclase (GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2). We have examined the tissue spcificity of its action and the relation of its action to those of the 8-bromo analogues of cyclic GMP and cyclic AMP. Heat-stable enterotoxin stimulated guanylate cyclase activity and increased cyclic GMP concentration throughout the small and large intestine. It increased transepithelial electric potential difference and short-circuit current in the jejunum, ileum and caecum but not in the duodenum or distal colon. This pattern of electrical responses was mimicked by 8-bromo-cyclic GMP. However, 8-bromo-cyclic AMP produced an electrical response in all intestinal segments. The enterotoxin failed to stimulate guanylate cyclase inliver, lung, pancreas or gastric antral mucosa. In the intestines, it stimulated only the particulate and not the soluble form of the enzyme. Preincubation of the toxin with intestinal membranes did not render it capable of stimulating pancreatic guanylate cyclase. Cytosol factors did not enhance the toxin's stimulation of intestinal guanylate cyclase. This study supports the role of cyclic GMP as intracellular mediator for heat-stable enterotoxin and suggests that the toxin affects a membrane-mediated mechanism for guanylate cyclase activation that is unique to the intestines.

Animals↗