SEARCH · PubMed Health

Results for “ENTEROTOXINS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

PubMed1989

Campylobacter jejuni chromosomal sequences that hybridize to Vibrio cholerae and Escherichia coli LT enterotoxin genes.

Campylobacter jejuni is one of the main etiologic agents of gastrointestinal illness in developing and developed areas throughout the world. Isolation of enterotoxin-producing C. jejuni has been associated with clinical symptoms of a watery-secretory type of diarrhea. Although physiological and immunological relatedness has been demonstrated between the C. jejuni enterotoxin (CJT), the Vibrio cholerae enterotoxin (CT), and the heat-labile cholera-like Escherichia coli enterotoxin (LT), nucleotide sequence similarity between C. jejuni DNA and either the toxA, toxB, eltA or eltB genes remained to be shown. We found that binding to ganglioside GM1 prevented recognition of CJT by monoclonal antibodies directed to either CT or LT. This indicates antigenic similarity between the three enterotoxins in the ganglioside GM1-binding site. Therefore we searched for corresponding similarities at the DNA level and found, by oligodeoxynucleotide hybridization, C. jejuni chromosomal nucleotide sequences similar to the coding region for a postulated ganglioside GM1-binding site on toxB and eltB.

Amino Acid Sequence↗

PubMedDate not supplied

High-level expression and secretion of a lysine-containing analog of Escherichia coli heat-stable enterotoxin.

The mechanism of action of the heat-stable enterotoxin STa secreted from enterotoxigenic forms of Escherichia coli has remained elusive, in part due to a tedious, low-yield purification procedure. We report here a method for obtaining large amounts of a biologically active lysine-containing analog of STa. Initial attempts to express the toxin using an expression vector that did not encode a signal sequence resulted in no biologically active material being recovered either from lysed cells or as a secretory product. However, use of the secretion vector pJAL36, which contains the STII enterotoxin signal sequence, allowed large amounts of an STa derivative containing the additional sequence Ser-Thr-Lys at the amino terminus of the mature enterotoxin to be readily purified from culture supernatants. This enterotoxin analog, known as KSTa-1, was equal in biological and receptor binding activity to the native toxin STa. The lysine residue present in KSTa-1 promises to be useful as a reactive amino acid that is readily derivatized to allow coupling of the enterotoxin to supports for affinity chromatography and antigenic conjugates. Additionally, the insertion of the lysine residue carboxy terminal to the Ser-Thr sequence adds a reversible "handle" to the toxin sequence in that the Ser-Thr-Lys segment can be removed by treatment with trypsin, releasing the native form of STa.

Amino Acid Sequence↗

PubMed1976

Enterotoxin testing of Escherichia coli causing epidemic infantile enteritis in the U.K.

Three test systems were used to study enterotoxin production by epidemic strains of Escherichia coli from cases of infantile enteritis in well-documented outbreaks in the U.K. The tests used were the Y1-mouse-adrenal-cell test and the Chinese-hamster-ovary-cell (C.H.O.) test for the detection of heat-labile enterotoxin and the infant-mouse test for the detection of heat-stable enterotoxin. All 6 outbreaks had been studied using full serotyping techniques and the results had been published. In each outbreak the epidemiological studies clearly implicated a particular serotype of E. Coli as the epidemic strain and cultures of that serotype were tested for enterotoxin production. Although a control strain validated by other workers was positive in all three systems, the epidemic strains from infantile enteritis were negative. It seems that the three enterotoxin tests used in this study are of little value in recognising strains of E. coli causing epidemics of infantile enteritis in the U.K.

Animals↗

PubMed1998

Immunostimulatory activity of LT-IIa, a type II heat-labile enterotoxin of Escherichia coli.

Certain bacterial molecules potentiate immune responses to parenterally administered antigens. One such molecule that has been intensely investigated is cholera toxin, a type I heat-labile enterotoxin produced by the Gram-negative bacterium Vibrio cholerae. Immunization with a mixture of a foreign antigen and cholera toxin enhances the immune response to the antigen. Similar adjuvant activity is associated with LT-I, a closely related type I heat-labile enterotoxin produced by Escherichia coli. The adjuvant activities of LT-IIa, a member of the type II heat-labile enterotoxins produced by E. coli, have not been described. LT-IIa and CT differ significantly in amino acid sequence of the B polypeptides and in receptor binding affinity. In this study, rats were subcutaneously immunized with fimbrillin, a protein isolated from the bacterium Porphyromonas gingivalis, and with fimbrillin in combination with LT-IIa, the prototypical type II enterotoxin. Previous studies documented that fimbrillin administered alone is a poor immunogen. Animals immunized with the mixture of fimbrillin and LT-IIa produced high titers of specific IgG antibody directed against fimbrillin. Anti-fimbrillin antibody titers in sera from animals receiving the combination of LT-IIa + fimbrillin were comparable to those obtained from sera of animals immunized with cholera toxin + fimbrillin. The results of these experiments demonstrate that LT-IIa exhibits an adjuvant activity that is equal to that of cholera toxin. Recombinant methods have been established for producing large amounts of LT-IIa, an advantage that will likely provide an economic impetus to consider incorporating the enterotoxin as an immunostimulatory agent in future vaccines.

Adjuvants, Immunologic↗

PubMed1999

Production and characterization of anti-peptide monoclonal antibodies with specificity for staphylococcal enterotoxins A and B.

A synthetic peptide containing selected epitopes from staphylococcal enterotoxin A (SEA) and enterotoxin B (SEB) was used to produce monoclonal antibodies (Mabs) to respective enterotoxins in a single fusion procedure. The peptide inhibited the reaction of polyclonal anti-SEA or anti-SEB antisera with their homologous enterotoxin, thus showing that the chosen epitopes are part of the antibody-inducing enterotoxin sequences. Two Mabs, Mab-A and Mab-B, reacted with both the peptide and with either SEA or SEB. Used in a double antibody sandwich ELISA, the Mabs were able to quantitate the native SEA or SEB toxins at nanogram levels.

Animals↗

PubMed2001

Prevalence of Staphylococcus aureus and staphylococcal enterotoxins in raw pork and uncooked smoked ham--a comparison of classical culturing detection and RFLP-PCR.

In many countries Staphylococcus aureus is considered to be the second or third most common pathogen causing outbreaks of food poisoning, only outnumbered by Salmonella spp. and in competition with Clostridium perfringens. Often the consumption of ham or meat containing staphylococcal enterotoxins (SE) is identified as cause of the illness. Thus, to gain an insight into the prevalence of S. aureus and its emetic enterotoxins in raw pork and uncooked smoked ham and to investigate how the prevalence of the pathogen is influenced during the fabrication process, a total of 135 samples of raw pork, salted meat and ready-for-sale uncooked smoked ham were examined for the prevalence of S. aureus and staphylococcal enterotoxins A to D (SEA-SED). To this means classical cultural methods were employed as well as molecular biological techniques (PCR) and the results were compared. In 25.9% of all samples S. aureus was detected by culture whereas 51.1% of the samples showed a positive result when PCR was used for the detection of the pathogen. Fresh meat was contaminated most often. By PCR, 62.2% were identified as being S. aureus positive compared to 57.7% positive samples using the cultural technique. The detection rate during the fabrication process declined significantly. The pathogen was cultivated from 8.9% of the salted meat samples. Here, 55.6% of the samples reacted positively in the PCR, and finally, in approximately a third of the ready-for-sale smoked hams, S. aureus genes were found. From 11.1% of these samples, the pathogen could be isolated by culture. From these results, we conclude that the PCR used in this study is more sensitive than the classical cultural method. By PCR, one or more staphylococcal enterotoxin genes were found in 24 of the 135 examined samples. This means that 34.8% of the staphylococcal strains identified using the PCR technique were enterotoxigenic. Using the SET-RPLA, a percentage of 28.6% enterotoxigenic isolates was ascertained. No staphylococcal enterotoxin formation was detected by the SET-RPLA in ready-for-sale ham, although SE-genes were found by PCR. The detection of SE-genes by PCR is faster and easier to perform than the SET-RPLA.

Animals↗

PubMed1989

Immune response to toxic-shock-syndrome toxin-1 (TSST-1) and to staphylococcal enterotoxins A, B and C in Staphylococcus aureus infections.

Isolates from 100 monomicrobial Staphylococcus aureus infections were tested for the production of TSST-1 and the enterotoxins A, B and C, which were found to be synthesized as a single toxin in 34 strains, or in combination of two or more toxins in 26. Acute phase sera and one or two further serum samples from 60 patients with toxigenic (either enterotoxins and/or TSST-1) S. aureus isolates were tested for humoral immune responses. Such immune responses occurred more frequently in septicemic than in localized staphylococcal infections, and more frequently against TSST-1 and the other enterotoxins than against enterotoxin A. Furthermore, the data suggest an immunological non-responsiveness to enterotoxin A in a considerable portion of the patients. The retrospective screening of the records of 15 selected patients for symptoms of Toxic-Shock-Syndrome revealed one case of probable TSS.

Adolescent↗

PubMed1985

Growth and enterotoxin production of Staphylococcus aureus in shrimp.

Strains of Staphylococcus aureus isolated from shrimp were examined for phage pattern and enterotoxin production; 63% of the strains isolated from North Sea shrimp were typable with the International and additional set of phages, as were 38% of the strains isolated from South-East Asian shrimp. Staphylococcal enterotoxin(s) (SE) were produced by 48% and 35% of strains isolated from North Sea and South-East Asian shrimp respectively. Growth and enterotoxin production by S. aureus in shrimp was examined in storage experiments at 22 degrees C. S. aureus increased by 1-2 log units in 24 h when the organism was only a minor part of the total microflora of shrimp. When S. aureus was an equivalent part of the total flora its numbers increased by 3-4 log units in 24 h. Enterotoxins A and B became detectable when the number of S. aureus exceeded 10(7) per g in aseptically peeled shrimp. Results indicate that S. aureus is able to produce enterotoxin in shrimp, but its production depends upon a number of factors, including the relationship between S. aureus and competitive micro-organisms. It is concluded that the presence of S. aureus on commercially produced shrimp represents a potential hazard to health.

Animals↗

PubMed2002

Helichrysum italicum extract interferes with the production of enterotoxins by Staphylococcus aureus.

AIMS: The purpose of this work was to evaluate the effect of Helichrysum italicum extract on enterotoxin (A-D) production by Staphylococcus aureus strains. METHODS AND RESULTS: The production of enterotoxins A-D in the presence or absence of H.italicum diethyl ether extract was estimated in microtiter plates using a reversed passive latex agglutination (SET-RPLA) kit (Oxoid, Basingstoke, UK). The results indicate that, in culture medium, inhibition of staphylococcal growth and enterotoxins appeared with 250-125 microg ml(-1) of the extract. Lower concentrations of the extract (62.5-31.25 microg ml(-1)) did not affect the final viable count of Staph. aureus but reduced the production of enterotoxins B and C. CONCLUSIONS: H. italicum interferes with growth and production of enterotoxins by Staph. aureus. SIGNIFICANCE AND IMPACT OF THE STUDY: There is considerable interest in the use of natural compounds as alternative methods to control undesirable pathogenic micro-organisms.

Asteraceae↗

PubMed1978

Heat-stable enterotoxin of Escherichia coli: in vitro effects on guanylate cyclase activity, cyclic GMP concentration, and ion transport in small intestine.

A partially purified preparation of the heat-stable enterotoxin of Escherichia coli caused a rapid and persistent increase in electric potential difference and short-circuit current when added in vitro to the luminal surface of isolated rabbit ileal mucosa. As little as 1 ng/ml produced an easily detectable response. Under short-circuit condition, the enterotoxin abolished net Cl- absorption; this change was half that produced by theophylline, which stimulated net secretion. The enterotoxin did not change cyclic AMP concentration but caused large and persistent increases in cyclic GMP concentration. The electrical and nucleotide responses exhibited similar and unusually broad concentration-dependences and maximal effects could not be demonstrated. Theophylline elevated cyclic GMP concentration 3-fold both in the presence and absense of the enterotoxin, suggesting no effect of the toxin on cyclic GMP phosphodiesterase. Guanylate cyclase [GTP pyrophosphatelyase(cyclizing); EC 4.6.1.2] activity in a crude membrane fraction from intestinal epithelial cells was stimulated 7-fold by the enterotoxin. These results suggest that guanylate cyclase stimulation is the basis for the toxin's diarrheagenic effect.

Bacterial Toxins↗

PubMed1997

Lck-independent triggering of T-cell antigen receptor signal transduction by staphylococcal enterotoxins.

Superantigens (SAgs) activate T-cells in a manner specific to the Vbeta region of the T-cell antigen receptor. Stimulations by SAgs provoke drastic T-cell activation that leads to programmed cell death or the anergic state of responding cells. To characterize the signal transduction pathway initiated by SAgs, mutant lines derived from the human leukemic T-cell line Jurkat were tested for their reactivities against prototypic SAgs, staphylococcal enterotoxins. The J.CaM1.6 cell line, which lacks Lck expression and lost reactivity against T-cell antigen receptor-mediated stimulation, was activated by staphylococcal enterotoxins in a manner indistinguishable from the Jurkat cell line. In contrast, the J.45. 01 cell line, which lacks expression of functional CD45, showed severely impaired reactivity. The role of Lck appears to be replaced by another Src family protein-tyrosine kinase, Fyn. In J.CaM1.6 cells, Fyn was rapidly phosphorylated and activated after staphylococcal enterotoxin treatment. The kinase-inactive mutant of Fyn significantly suppressed the reactivity against staphylococcal enterotoxin E in J.CaM1.6 cells, and the expression of the active form of Fyn reconstituted reactivity against staphylococcal enterotoxin E in J.45.01 cells. These results demonstrate that SAgs activate T-cells in an Lck-independent pathway and that Fyn plays a critical role in the process.

Antigens, CD↗

PubMed1979

The molecular mode of action of Clostridium perfringens enterotoxin.

While certain strains of Clostridium perfringens have been associated with food poisoning outbreaks for the past 30 years, it has been only during the past 10 years that progress has been made in describing the disease process. And only within the past 5 years has meaningful progress been made in understanding the mechanism by which the disease is caused. Early observations, that the protein enterotoxin can cause erythema, increase capillary permeability, and exhibit parasympathomimetic properties, have been greatly added to in more recent studies. It is now believed tht the enterotoxin can alter intestinal transport of fluid, ions, and glucose, cause tissue damage in the gut and inhibit metabolic processes in intestinal tissue. Furthermore, the enterotoxin is thought to act very quickly (in a matter of minutes, compared to hours for other known enteropathogenic factors) and to affect basic function (macromolecular synthesis) and structure (membrane damage to microvillus brush borders) of individual cells. These findings have opened up many new questions that hopefully, when answered, will further the understanding of how this enterotoxin acts, as well as other enterotoxins being studied today.

Animals↗

PubMedDate not supplied

Modes of action of enterotoxins from Vibrio cholerae and EScherichia coli.

Current information on the intestinal secretory mechanism and on the actions of the enterotoxins from Vibrio cholerae and Escherichia coli are reviewed. These enterotoxins, through their effects on the metabolism of cyclic nucleotides, both inhibit active absorption and stimulate active secretion of water and electrolytes in the small intestine. the enterotoxin of V. chol erae and the heat-labile enterotoxin of E. coli affect these activities by stimulating adenylate cyclase, and the heat-stable enterotoxin of E. coli does so by stimulating guanylate cyclase.

Adenosine Monophosphate↗

PubMed1990

Immunobiological relationships of the enterotoxins produced by cholera toxin gene-positive (CT+) and -negative (CT-) strains of Vibrio cholerae O1.

The optimum rabbit ileal loop (RIL) reacting doses of the new cholera toxin (NCT) produced by cholera toxin gene-negative (CT-) strain X-392 and of the enterotoxin produced by cholera toxin gene-positive (CT+) strain 569B of Vibrio cholerae O1 were found to be 32 micrograms and 22 micrograms respectively. Production of NCT by the CT+ strain, in addition to CT, was confirmed by in-vivo neutralisation tests. Anti-569B-enterotoxin neutralised the optimum RIL reacting activity of NCT completely at 1 in 16 dilution, whereas the activity of 569B enterotoxin was only partially neutralised (44%) by anti-NCT. Similarly, partial neutralisation (66%) was observed when purified anti-CT was mixed with 569B enterotoxin. Therefore, the fluid accumulation produced in the RIL by 569B enterotoxin was the combined effect of both CT and NCT. No antigenic relationship between NCT and CT could be demonstrated in gel-diffusion tests.

Animals↗

PubMed1995

No difference in enterotoxin production among Staphylococcus aureus strains isolated from blood compared with strains isolated from healthy carriers.

The production of enterotoxin A, B, C and D by 196 Staphylococcus aureus strains isolated from blood cultures and 95 strains from nasal carriers was investigated. Half of the bacteraemia strains were from patients who died with or because of their infection, the other half from patients who survived. The nasal strains were selected to match the bacteraemia strains regarding phage types. Overall, 30.6% of the bacteraemia strains and 40.0% of the nasal strains produced enterotoxins; enterotoxins B and C were the toxins produced most frequently in both groups. A similar incidence and pattern of enterotoxin production was found among the bacteraemia strains of S. aureus regardless of acquisition of the infection, the portal of entry, presence or absence of endocarditis and outcome of the infection. Thus, the concept that the enterotoxins play an important role in staphylococcal infections, apart from the diseases caused by the toxins per se such as food poisoning and toxic shock syndrome, cannot be substantiated by the results of the present study.

Bacteremia↗

PubMed1999

Cationic currents induced by Clostridium perfringens type A enterotoxin in human intestinal CaCO-2 cells.

Clostridium perfringens type A produces an enterotoxin that induces diarrhoea experimentally in man and animals. The enterotoxin causes increased membrane permeability in susceptible cells which is thought to be due to pore formation in the host cell membrane. The effect of purified C. perfringens enterotoxin on intact intestinal CaCO-2 monolayers was examined in Ussing chambers and on single cells by whole-cell patch clamp. Mucosal application of C. perfringens enterotoxin resulted in prompt increases in short-circuit current coupled with a reduction in transepithelial resistance consistent with movement of sodium and other cations smaller than diethanolamine from mucosa to serosa. These changes were independent of extracellular calcium. Increases in short-circuit current were also observed in the apical membranes of CaCO-2 monolayers permeabilised across the basolateral membrane with nystatin. Currents were blocked by subsequent exposure to mucosal barium and zinc. Zinc also prevented the development of the current increases in apical membranes. Cationic currents were also observed following exposure of single CaCO-2 cells in whole-cell patch clamp recordings. These data indicate that C. perfringens enterotoxin is able to form cation permeant pores in the apical membrane of human intestinal CaCO-2 epithelia and the increases in short-circuit current can be prevented by pre-exposure to zinc ions.

Caco-2 Cells↗

PubMed2003

Detection of Clostridium difficile cytotoxin and Clostridium perfringens enterotoxin in cases of diarrhoea in the community.

Faecal specimens from 843 cases of diarrhoea in the community were tested for the presence of Clostridium difficile cytotoxin and Clostridium perfringens enterotoxin. C. difficile cytotoxin was detected in faecal specimens from 0.6 % of cases aged at least 2 years by using a Vero cell assay. Factors associated with detection of C. difficile cytotoxin were antibiotic therapy, age over 60 years and living in a home with other elderly people. Three methods were used for the detection of C. perfringens enterotoxin: a Vero cell assay, a commercial (TechLab) enzyme immunoassay (EIA) and an in-house EIA. The lower level of detection of pure C. perfringens enterotoxin in buffer was 0.01 micro g ml(-1) by the TechLab EIA and 1.0 micro g ml(-1) by the Vero cell assay. C. perfringens enterotoxin was detected by using the TechLab EIA in faecal specimens from 2.5 % of cases. This commercial EIA was less sensitive than the in-house EIA, detecting only 31 % of positive cases, but was specific and could be used for outbreak investigation by routine diagnostic laboratories. Age over 60 years was a factor associated with C. perfringens enterotoxin detection; this age group may be targeted for testing.

Adolescent↗

PubMed1995

Role of a potential endoplasmic reticulum retention sequence (RDEL) and the Golgi complex in the cytotonic activity of Escherichia coli heat-labile enterotoxin.

Recent experimental evidence indicates that Escherichia coli heat-labile enterotoxin and the closely related cholera toxin gain access to intracellular target substrates through a brefeldin A-sensitive pathway that may involve retrograde transport through the Golgi-endoplasmic reticulum network. The A subunits of both toxins possess a carboxy-terminal tetrapeptide sequence (KDEL in cholera toxin and RDEL in the heat-labile enterotoxins) that is known to mediate the retention of eukaryotic proteins in the endoplasmic reticulum. To investigate the potential role of the RDEL sequence in the toxic activity of the heat-labile enterotoxin we constructed mutant analogues of the toxin containing single substitutions (RDGL and RDEV) or a reversed sequence (LEDR). The single substitutions had little effect on Chinese hamster ovary cell elongation or the ability to stimulate cAMP accumulation in Caco-2 cells. Reversal of the sequence reduced the ability of the toxin to increase cAMP levels in Caco-2 cells by approximately 60% and decreased the ability to elicit elongation of Chinese hamster ovary cells. The effects of the heat-labile enterotoxin were not diminished in a mutant Chinese hamster ovary cell line (V.24.1) that belongs to the End4 complementation group and possesses a temperature-sensitive block in secretion that correlates directly with the disappearance of the Golgi stacks. Collectively, these findings suggest that the brefeldin A-sensitive process involved in intoxication by the heat-labile enterotoxin does not involve RDEL-dependent retrograde transport of the A subunit through the Golgi-endoplasmic reticulum complex. The results are more consistent with a model of internalization involving translocation of the A subunit from an endosomal or a trans-Golgi network compartment.

Amino Acid Sequence↗