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PubMed2001

Induction of apoptosis in HT29 human intestinal epithelial cells by the cytotoxic enterotoxin of Aeromonas hydrophila.

The cytotoxic enterotoxin produced by Aeromonas hydrophila is considered to be the main virulence factor in gastrointestinal infections mediated by this pathogen. In this study, we examined the morphological and apoptotic effects of this toxin on HT29 cells, using light and electron microscopy in situ, as well as agarose gel electrophoresis of cell DNA. Cells treated with the cytotoxic enterotoxin became round and lost their polarity as well as their adhesion to each other and to the substrate. Cytoplasmic blebbing and nuclear condensation also occurred. DNA fragmentation was detected by TUNEL labelling and agarose gel electrophoresis. These results show that the cytotoxic enterotoxin of A. hydrophila can induce apoptosis in human intestinal cells in culture.

Aeromonas hydrophila↗

PubMed1992

Stimulation of intestinal Cl- transport by heat-stable enterotoxin: activation of cAMP-dependent protein kinase by cGMP.

Heat-stable enterotoxins activate guanylate cyclase, whereas heat-labile enterotoxins stimulate adenylate cyclase. Both classes of toxins cause secretory diarrhea at least in part by stimulating Cl- secretion in the intestine. The mechanism for regulation of Cl- secretion by guanosine 3',5'-cyclic monophosphate (cGMP) was investigated using cultured T84 intestinal cells as a model for intestinal crypt cells. Escherichia coli heat-stable enterotoxin (ST) markedly stimulated cGMP production in T84 cells. Cl- secretion across T84 cell monolayers cultured on permeable filters was stimulated by E. coli ST, cholera toxin, or 8-BrcAMP, but 8-BrcGMP was ineffective. cGMP analogues that are known to be potent and specific activators of cGMP-dependent protein kinase (cG-kinase) also had little effect on 36Cl- uptake by T84 cells cultured in plastic dishes. E. coli ST, forskolin, cholera toxin, or membrane-permeant cAMP analogues markedly increased 36Cl- uptake into T84 cells. The general protein kinase inhibitor, staurosporine, inhibited the stimulation of Cl- permeability elicited by E. coli ST, vasoactive intestinal peptide (VIP), or 8-BrcAMP. DEAE-Sephacel chromatography revealed a predominant type II isoform of cAMP-dependent protein kinase (cA-kinase) in T84 cells, whereas little or no cytosolic cG-kinase activity was found. Treatment of T84 cells with E. coli ST or VIP resulted in an increase in the cA-kinase activity ratio (-cAMP/+cAMP) if the cytosolic enzyme was assayed at reduced temperature (on ice).(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport↗

PubMed2000

Inhibition of enterotoxin-induced porcine colonic secretion by diarylsulfonylureas in vitro.

Muscle-stripped piglet colon was used to evaluate changes in short-circuit current (I(sc)) as an indicator of anion secretion. Mucosal exposure to Escherichia coli heat-stable (STa) or heat-labile enterotoxins (LT) stimulated I(sc) by 32 +/- 5 and 42 +/- 7 microA/cm(2), respectively. Enterotoxin-stimulated I(sc) was not significantly affected by either 4,4'-diaminostilbene-2, 2'-disulfonic acid or CdCl(2), inhibitors of Ca(2+)-activated Cl(-) channels and ClC-2 channels, respectively. Alternatively, N-(4-methylphenylsulfonyl)-N'-(4-trifluoromethylphenyl)urea (DASU-02), a compound that inhibits cystic fibrosis transmembrane conductance regulator (CFTR)-mediated Cl(-) secretion, reduced I(sc) by 29 +/- 7 and 34 +/- 11 microA/cm(2), respectively. Two additional diarylsulfonylurea (DASU)-based compounds were evaluated for their effects on enterotoxin-stimulated secretion. The rank order of potency for inhibition by these three closely related DASU structures was identical to that observed for human CFTR. The degree of inhibition by each of these compounds was similar for both STa and LT. The structure- and concentration-dependent inhibition shown indicates that CFTR mediates both STa- and LT-stimulated colonic secretion. Similar structure-dependent inhibitory effects were observed in forskolin-stimulated rat colonic epithelium. Thus DASUs compose a family of inhibitors that may be of therapeutic value for the symptomatic treatment of diarrhea resulting from a broad spectrum of causative agents across species.

Amiloride↗

PubMed2005

Increased levels of serum-specific immunoglobulin e to staphylococcal enterotoxin a and B in patients with allergic rhinitis and bronchial asthma.

BACKGROUND: The association between staphylococcal enterotoxins and atopic dermatitis (AD) is well characterized. We aim to evaluate the association between sensitization to staphylococcal enterotoxin A (SEA) and/or B (SEB) and the development of allergic airway disease. METHODS: Two hundred and seventy-four patients were grouped into allergic rhinitis (AR) and/or bronchial asthma (BA) only, AD only and AR/BA+AD. The AR/BA only group was further divided into AR only, AR and airway hyperresponsiveness (AR+AHR) and BA. The allergen-specific and total immunoglobulin E (IgE) antibodies were determined by the CAP system. The associations of sensitization to SEA/SEB with allergic airway disease were analyzed by logistic regression analysis. RESULTS: The overall rate of sensitization to SEA/SEB was 25.7%, whereas the rate of the AD only group (45.5%) was significantly higher than that of the AR/BA only group (24.5%, chi2=8.1). After sensitization to SEA/SEB, the geometric mean total IgE levels were significantly elevated in patients with AR+AHR and BA, but not in those with AR only. BA patients had higher geometric mean values of SEA- and SEB-specific IgE than AR only and AR+AHR patients. Logistic regression revealed that AR/BA only was more associated with sensitization to SEA/SEB (odds ratio 6.57) than AD only and AR/BA+AD (odds ratio 2.44 and 1.72). CONCLUSIONS: Atopic status after sensitization to SEA/SEB was more closely associated with BA than with other airway allergy, implying that SEA/SEB may play a role in exacerbating airway allergy and increasing the risk of allergic airway disease. Our study suggests that staphylococcal enterotoxins play a prominent role in the pathogenesis of allergic airway disease as well as AD.

Adolescent↗

PubMed1973

Alkaline phosphatase. Possible induction by cyclic AMP after cholera enterotoxin administration.

The present studies were undertaken to determine the role, if any, of cyclic 3',5'-adenosine monophosphate (cyclic AMP) as a chemical inducer of rat liver alkaline phosphatase. Cholera enterotoxin, given intravenously to rats, led to a rapid rise in the activity of hepatic adenyl cyclase that was 7(1/2) times greater than control values in 6 h. Cyclic AMP levels were also significantly increased above control values while the activity of cyclic nucleotide phosphodiesterase was unchanged. Hepatic alkaline phosphatase activity was increased 5(1/2) times above control in 12 h, but its rise followed that of adenyl cyclase and cyclic AMP by several hours. Cycloheximide inhibited the rise of hepatic alkaline phosphatase but not that of adenyl cyclase. The administration of glucagon, a known stimulator of hepatic adenyl cyclase, and of dibutyryl cyclic AMP, led to similar striking increases in hepatic alkaline phosphatase activity. This alkaline phosphatase increase was blocked by the prior administration of cycloheximide. Bile duct ligation, a known stimulator of hepatic alkaline phosphatase activity, failed to produce any significant changes in adenyl cyclase or cyclic AMP. Concomitant treatment of rats with bile duct ligation and cholera enterotoxin or bile duct ligation and glucagon, had no additive effect on the increase in hepatic alkaline phosphatase activity, although the increase occurred earlier. These results suggest that: (a) cyclic AMP may act as an inducer of hepatic alkaline phosphatase: (b) the stimulation of hepatic alkaline phosphatase by cholera enterotoxin is mediated by cyclic AMP; (c) the rise in hepatic alkaline phosphatase following bile duct ligation is not mediated by cyclic AMP; (d) the same alkaline phosphatase in rat liver may be induced by two (or more) mechanisms, only one of which requires cyclic AMP.

Adenylyl Cyclases↗

PubMed1978

Activation of adenylate cyclase by heat-labile Escherichia coli enterotoxin. Evidence for ADP-ribosyltransferase activity similar to that of choleragen.

Highly purified, polymyxin-released, low molecular weight Escherichia coli heat-labile enterotoxin (LT) catalyzed the hydrolysis of NAD to ADP-ribose and nicotinamide. This NAD glycohydrolase activity was stimulated by dithiothreitol and was independent of cellular components. Nicotinamide formation was enhanced by arginine methyl ester > d-arginine congruent with l-arginine congruent with guanidine. A 20-fold increase in activity was noted with arginine methyl ester, and maximal activity again required dithiothreitol. When the reaction was initiated with toxin, a delay was observed before a constant rate was established. The reaction products found after incubation of [adenine-U-(14)C]NAD and l-[(3)H]arginine or unlabeled arginine methyl ester with the enterotoxin had mobilities on thin-layer chromatograms similar to the reaction products obtained after incubation of choleragen with these substrates and are consistent with the formation of ADP-ribose-l-arginine and ADP-ribose-l-arginine methyl ester, respectively. Both toxins, which catalyze the NAD-dependent activation of adenylate cyclase, thus appear to possess NAD glycohydrolase and ADP-ribosyltransferase activities. Although the activities of both toxins are dependent on dithiothreitol, Escherichia coli enterotoxin exhibited optimal activity in Tris (Cl(-)) (pH 7.5) and was inhibited by high concentrations of potassium phosphate (pH 7.0) or low pH (sodium acetate, pH 6.2). It appears that the optimal assay conditions as well as the kinetic constants for the reactants differ from those previously noted with choleragen. It is probable therefore that although the two toxins catalyze similar reactions, they differ in primary structure. The presence of transferase and glycohydrolase activities in structurally distinct toxins that activate adenylate cyclase strengthens our hypothesis that the ADP-ribosylation of arginine is a model for the NAD-dependent activation of adenylate cyclase; activation may result from ADP-ribosylation of the cyclase itself or of a protein that regulates its activity.

Adenosine Diphosphate Sugars↗

PubMed1979

Gangliosides sensitize unresponsive fibroblasts to Escherichia coli heat-labile enterotoxin.

Chemically transformed mouse fibroblasts did not raise their cyclic AMP level in response to Escherichia coli heat-labile enterotoxin. These fibroblasts did, however, incorporate exogenous mono-, di-, and trisialogangliosides. After the uptake of monosialoganglioside galactosyl-N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylglucosylceramide (GM1), the cells responded to E. coli heat-labile enterotoxin. The di- and trisialogangliosides were considerably less effective. GM1, the putative cholera toxin (choleragen) receptor, has been implicated previously as the receptor for E. coli heat-labile enterotoxin based on the ability of the free ganglioside to inhibit the effects of toxin. This investigation establishes that the ganglioside, when incorporated into fibroblasts, serves a functional role in mediating the responsiveness to the toxin.

Animals↗

PubMed1988

Mechanism of action of Escherichia coli heat stable enterotoxin in a human colonic cell line.

Escherichia coli heat stable enterotoxin (STa) caused Cl- secretion across T84 cell monolayers in a dose-dependent manner only when applied to the apical membrane surface and not when applied to the basolateral surface. Measurement of cAMP, cGMP, and free cytosolic Ca2+ in response to STa suggested that cGMP alone mediated the Cl- secretory response. Studies utilizing blockers of the Na+,K+-ATPase pump, a Na+,K+,Cl- cotransport system, a K+ channel, and a Cl- channel suggest that all of them participate in the Cl- secretory process induced by STa. The results suggest that the Cl- secretory response induced by STa is mediated by cGMP after the enterotoxin binds to its receptor on the apical membrane. The enterotoxin, by increasing cGMP, opens a K+ channel on the basolateral membrane as well as a Cl- channel on the apical membrane. The activation of these ion exit mechanisms, together with activations of the Na+,K+,Cl- cotransporter and the Na+,K+-ATPase pump drives Cl- exit through the Cl- channel on the apical membrane.

Bacterial Toxins↗

PubMed1991

Enteroaggregative Escherichia coli elaborate a heat-stable enterotoxin demonstrable in an in vitro rabbit intestinal model.

Enteroaggregative Escherichia coli (EAggEC) have been associated with persistent diarrhea in young children, but little is known about its pathogenesis. We assayed for enterotoxic activity in culture filtrates (CF) of EAggEC strains in Ussing chambers mounted with rabbit ileal mucosa. CF from strain 17-2, a prototype Chilean EAggEC strain, caused a greater rise in potential difference and short circuit current (SCC) than that seen in HB101 control, and this effect was abolished by protease pretreatment and partially stable after heat treatment. Ultrafiltration of 17-2 CF preparations localized the active moiety to the 2-5 kD Mr size range. CF from HB101 transformed with the 17-2 plasmid showed Ussing chamber activity. less than 10-kD CF fractions from five of six other EAggEC strains screened in Ussing chambers gave SCC responses of similar magnitude to 17-2. The 17-2 CF activity was not neutralized after pretreatment with polyclonal anti-STa antibody. Additionally, all of the seven EAggEC strains studied were nonreactive by heat-stable enterotoxin variant STa ELISA, were negative in the suckling mouse assay, and failed to hybridize with heat-stable enterotoxin variant STh and STp DNA probes. In summary, our data indicate that 17-2 produces a low molecular weight, partially heat-stable, protease-sensitive enterotoxin which appears to be plasmid associated, and genetically and immunologically distinct from E. coli STa. Preliminary screening suggests that this tox+ phenotype may be common among EAggEC.

Animals↗

PubMed2006

Comparative inflammatory properties of staphylococcal superantigenic enterotoxins SEA and SEG: implications for septic shock.

The severity of Staphylococcus aureus sepsis is positively associated with staphylococcal enterotoxin A (SEA) and negatively associated with the enterotoxin gene cluster (egc), which encodes five staphylococcal enterotoxins. We postulated that the variable, clinical severity of S. aureus sepsis might be a result of differences in the inflammatory properties of staphylococcal superantigens. We therefore compared the inflammatory properties of SEA with those of staphylococcal entérotoxin G (SEG), a member of the five egc superantigens. We found that SEA and SEG had similar superantigenic properties, as they induced CD69 expression on T lymphocytes and selective expansion of Vbeta subpopulations. Contrary to SEG, however, SEA induced a strong proinflammatory/Th1 response, including TNF-alpha and MIP-1alpha production. These results suggest that the association of SEA with the severity of S. aureus septic shock, characterized by a deleterious, inflammatory cascade, may be explained partly by the specific proinflammatory properties of this superantigen.

Antigens, CD↗

PubMed1986

Carryover of preformed staphylococcal enterotoxins and thermostable deoxyribonuclease from raw cow milk to Khoa--a heat-concentrated Indian milk product.

Preformation of enterotoxins and thermostable deoxyribonuclease by Staphylococcus aureus in raw cow milk and their carryover to Khoa--a heat-concentrated (98 degrees C for 15 to 20 min) Indian milk product--was evaluated. Detectable enterotoxins and deoxyribonuclease, as evidenced in the zone diameters of 10 to 16 mm, were performed in 10 h incubation of milk samples inoculated with strains of Staphylococcus aureus at 1 X 10(6) cfu/ml of milk. Both preformed enterotoxins and thermostable deoxyribonuclease were carried over to Khoa from raw milk. The study implies the use of good quality raw milk free from pathogenic organisms for preparation of milk products such as Khoa.

Animals↗

PubMed2004

Laboratory exposures to staphylococcal enterotoxin B.

Staphylococcal enterotoxins are 23- to 29-kDa polypeptides in the bacterial superantigen protein family. Clinical symptoms from intoxication with staphylococcal enterotoxins vary by exposure route. Ingestion results in gastrointestinal symptoms, and inhalation results in fever as well as pulmonary and gastrointestinal symptoms. Review of occupational exposures at the U.S. Army Medical Research Institute of Infectious Diseases from 1989 to 2002 showed that three laboratory workers had symptoms after ocular exposure to staphylococcal enterotoxin B (SEB). Conjunctivitis with localized cutaneous swelling occurred in three persons within 1 to 6 hours after exposure to SEB; two of these persons also had gastrointestinal symptoms, which suggests that such symptoms occurred as a result of exposure by an indirect cutaneous or ocular route. Ocular exposures from SEB resulting in conjunctivitis and localized swelling have not previously been reported. Symptoms from these patients and review of clinical symptoms of 16 laboratory-acquired inhalational SEB intoxications may help healthcare workers evaluate and identify SEB exposures in laboratory personnel at risk.

Accidents, Occupational↗

PubMed2002

Inhibition of growth, enterotoxin production, and spore formation of Clostridium perfringens by extracts of medicinal plants.

The extracts of 14 plants used in the traditional medicine of Mexico were evaluated for their effects on the growth, spore formation, and enterotoxin production of Clostridium perfringens type A. The extracts of Psidium guajava L., Haemotoxylon brasiletto, and Euphobia prostata were the most effective inhibitors of growth, spore formation, and enterotoxin production. No enterotoxins were detected when extracts were added to the media at less than the MIC for growth.

Clostridium perfringens↗

PubMed1978

Enterotoxin-producing Escherichia coli and diarrhoea among newborn babies in Darwin.

Specimens of Escherichia coli O119B14 isolated from 13 newborn babies during an outbreak of diarrhoea in Darwin Hospital were tested for their ability to produce enterotoxin. Of the 13 isolates tested none was found to produce heat-labile enterotoxin. However, isolates from two of the five diarrhoeal faecal specimens were found to produce moderate levels of heat-stable enterotoxin (ST). It seems like that ST-producing strains of E. coli were responsible for the diarrhoea.

Australia↗

PubMed1997

[Analysis of antibiotic resistance and production of enterotoxin of MRSA].

100 separate Staphylococcus aureus (S. a) isolates at Beijing Jishuitan Hospital during Oct. 1994-Apr. 1995 were submitted to determine the proportion of methicillin-resistant S. a (MRSA) and susceptibility test to 12 antibiotics. MIC determinations of the antibiotics were performed. Also, production rate of enterotoxin was measured with RPLA method. The results showed that MRSA constituted 60% of all cultures. (Burns Dept. 67.4%, Internal Medicine 62.5%, Orthopedics Dept. 44%). The antibiotics with resistant rate of MRSA below 50% included vancomyin (3.3%), norvancomyin (5%) and amikacin (21.5%). The production rate of enterotoxin was 100% in MRSA and 20% in MSSA (methicillin-sensitive S. a). In this group, 35% of MRSA and 5% of MSSA produced more than 2 types of enterotoxin.

Anti-Bacterial Agents↗

PubMed1999

Induction of Salmonella enterotoxin (stn) gene expression by epithelial cells (IEC-6).

Prevalence of Salmonella enterotoxin (stn) gene among Salmonella enterica and S. bongori was investigated by polymerase chain reaction (PCR) and gene probe and its status of phenotypic expression was examined on chinese hamster ovary cells by cultivating the strains with conventional method for enterotoxin production and by cultivating the organisms in contact with intestinal epithelial cells of rats (IEC-6). All the 19 strains and serovars of S. enterica such as Typhimurium, Enteritidis, Newport, Weltevreden, Indiana, Gallinarum and Kentucky were found to carry stn gene as examined by PCR and gene probe but only a limited number of strains (13 out of 19) expressed phenotypically the enterotoxin when cultured by conventional method. Cultivation of organisms in contact with epithelial cells induced expression of stn gene phenotypically in all the 19 strains. In contrast to S. enterica, strains of S. bongori were found neither genotypically (stn) nor phenotypically (Stn) positive.

Animals↗

PubMed1999

Gene fusion and expression of heat-labile and heat-stable enterotoxins of enterotoxigenic Escherichia coli.

The vaccine candidate comprising the genes that code the B subunit of the heat-labile enterotoxin (LT-B) and the heat-stable enterotoxin (ST) of enterotoxigenic E. coli (ETEC) had been constructed by recombinant genetic techniques. The 5'terminus of the gene encoding pro-ST was genetically fused to the 3'terminus of the LT-B gene. The pro-ST gene containing mature ST sequence and pro sequence which codes for the pro region of ST precursors was amplified by PCR from pSLN004 plasmid. To reduce toxicity of the ST in vitro was substituted Leu for Ala residue at position 14 of ST by oligonucleotide-directed site mutagenesis. For this construction, the expression of ST antigenicity and LT antigenicity were obtained when a five amino-acid or a nine-amino-acid linker were included between the LT-B and pro-ST moieties. The LT-B/pro-ST fusion peptides possessed no enterotoxic activity of heat-stable and heat-labile enterotoxins, and retained the ability to bind GM1 ganglioside. More importantly, these LT-B/pro-ST fusion peptides were immunogenic. The preparations containing the hybrid molecule elicited special antibodies that were to recognize native toxin in vitro.

Animals↗

PubMed2000

[Interspecies lysogenization in staphylococci: transfer of bacteriophage converting enterotoxin A from a clinical strain of Staphylococcus aureus to Staphylococcus intermedius].

The ability of lysogenization was examined of 50 S. intermedius strains and of 77 strains belonging to 14 different species of coagulase-negative staphylococci using 8 enterotoxin A converting bacteriophages isolated from S. aureus. All the examined bacteriophages showed lytic activity against at least 1 of 11 susceptible strains of S. intermedius to them. Lytic activity towards coagulase-negative staphylococci was observed for 6 of 8 examined bacteriophages. Two bacteriophages were active against 1 of 9 examined S. capitis strains, one against 1 of 11 examined S. haemolyticus strains, four against 1 of 6 examined S. lugdunensis strains, three against 1 of 6 examined S. warneri strains and one against 1 of 5 examined S. xylosus strains. Lysogenization with bacteriophage f421-1 able to convert positively enterotoxin A and staphylokinase and negatively beta-haemolysin of one S. intermedius strain was successful. S. intermedius lysogenized with phi 421-1 was able to produce both enterotoxin A and staphylokinase and lost ability to produce beta-haemolysin. Our results showed a broad lytic spectrum and interspecies host range of some S. aureus bacteriophages and the ability of interspecies transfer of bacteriophages between S. aureus and S. intermedius.

Enterotoxins↗