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 1,387 records · Page 77Linked to original sources

PubMed1995

Staphylococcal enterotoxin B increases the severity of type II collagen induced arthritis in mice.

OBJECTIVE: To observe the influence of T cell subset changes on the development of experimental arthritis, by using the bacterial superantigen staphylococcal enterotoxin B (SEB) to modulate the T cell repertoire during the arthritogenic response to type II collagen (CII) in vivo. METHODS: DBA/1 mice were injected with SEB before immunisation with CII, and assessed for the development of collagen induced arthritis (CIA) and an immune response to CII. Mice with established arthritis were also treated therapeutically with SEB. Flow cytometry was used to evaluate the effect of the therapy on T cell subsets and T cell receptor (TCR) V beta expression. RESULTS: Mice injected with SEB developed arthritis significantly faster than saline treated control animals, and developed more severe clinical features. Mice treated with SEB after the onset of CIA were also observed to progress more rapidly to a severe arthritis than mice treated with saline alone. The level of anti-CII antibody was not affected by SEB injection. Flow cytometric analysis of TCR expression in mice 21 days after injection of CII showed decreased expression of V beta 6 and V beta 8 cells in SEB treated mice, compared with collagen immunised control mice. Injection of SEB alone caused a decrease in V beta 8, but not V beta 6 T cells compared with the values in normal DBA/1 mice. No significant variations in the T cell repertoire were detected 70 days after CII immunisation. CONCLUSIONS: Treatment with the bacterial enterotoxin SEB before the induction of arthritis did not suppress the immunological or arthritogenic response to CII in DBA/1 mice, despite the modulation of the V beta 8 T cell subset. Treatment of mice with established arthritis using SEB provoked a more severe disease course.

Animals↗

PubMed1994

Effect of Escherichia coli enterotoxins on macromolecular absorption.

Macromolecular absorption of gliadin, a wheat protein and alpha lactalbumin, a milk protein was evaluated in control and Escherichia coli enterotoxin (heat-stable, heat-labile, and both heat-stable and heat-labile enterotoxin) treated mice. The peak concentration of gliadin and lactalbumin was two hours and three hours after their ingestion, respectively. There was also a significant increase (p < 0.01) in the absorption of both the proteins in all the three toxin treated groups compared with the control group. These results suggest that intestinal permeability and macromolecular absorption changes after E coli infection.

Animals↗

PubMed1976

Detection of staphylococcal enterotoxin in gastric juice.

The gastric juice of a patient showing symptoms of staphylococcal food poisoning was examined by a radioimmunoassay for the presence of enterotoxins. Assays gave markedly higher results at 35 degrees than at 5 degrees. The source for this discrepancy was attributed to interference due to trypsin activity on the basis of (1) the demonstration of hydrolysis of p-toluenesulfonyl-L-arginine methyl ester by the specimen, (2) inhibition of this activity by trypsin inhibitor from lima bean, and (3) lowered values produced for enterotoxins in gastric juice when the inhibitor was included in the assay system.

Adult↗

PubMed1978

Evaluation of staphylococcal thermonuclease (TNase) assay as a means of screening foods for growth of staphylococci and possible enterotoxin production.

Samples of food, naturally and artificially contaminated with Staphylococcus aureus, were analyzed for enterotoxin and thermonuclease (TNase). With the exception of egg, all naturally contaminated foods with detectable amounts of staphylococcal enterotoxin were positive for TNase. The enzyme was also present in the majority of foods with over 1 million S. aureus cells per gram. In artificially contaminated foods. TNase was detected in all samples except egg, acidic foods in which growth of S. aureus was suppressed, and some samples of raw ground beef. Recovery of TNase was influenced by the type of food.

Enterotoxins↗

PubMed1986

Evaluation of radioimmunoassay performance for staphylococcal enterotoxin in foods: application of external quality assessment survey.

An external quality assessment survey for staphylococcal enterotoxin A, B, and C2 determinations was performed in the collaborative study. Three analysts in two laboratories took part. Three types of food, cheese, salami, and pasta, were artificially contaminated with either one toxin only or all three toxins. A total of 378 analyses were performed. The group mean of the analytical values corresponded fairly well to the given enterotoxin concentrations. However, a considerable interlaboratory imprecision was found despite analyses being performed with the same reagents and methodology.

Cheese↗

PubMed1986

Evaluation of the reversed passive latex agglutination (RPLA) test kits for detection of staphylococcal enterotoxins A, B, C, and D in foods.

Four lots of the SET-RPLA kit (Denka Seiken Co. Ltd., Tokyo), a commercial reverse passive latex agglutination test kit for the detection of staphylococcal enterotoxins A, B, C, and D in foods, have been evaluated for their efficacy. The kits showed high specificity and sensitivity with a detection limit of 0.75 ng enterotoxin/g of food. The test is simple, is completed within 24 h, and does not require complicated extraction or concentration procedures nor expensive equipment. In addition, the assay is semiquantitative. However, as in any other immunological system, routine verification of the specificity of the latex reagents against standard enterotoxins and toxin-free food extracts is necessary.

Enterotoxins↗

PubMed1991

Production and characterization of murine monoclonal antibodies against staphylococcal enterotoxins A and E.

Six murine monoclonal antibodies (MAbs) against staphylococcal enterotoxin A (SEA) and enterotoxin E (SEE) were prepared by fusion of myeloma cells with mouse spleen cells immunized with SEA and SEE. Of five MAbs to SEA tested, two MAbs were reactive with only SEA, whereas three were specific for both SEA and SEE. On the other hand, one MAb to SEE was found to be specific for only SEE. To study specificities of the combining sites of these MAbs, competitive binding assays with either SEA or SEE and horseradish peroxidase conjugated MAbs were performed using unconjugated MAbs as inhibitors. The results obtained in the assays suggest that different epitopes may be located on SEA and that some of them may be cross-reacting epitopes between SEA and SEE.

Animals↗

PubMed1980

Shigella dysenteriae I enterotoxin: proposed role in pathogenesis of shigellosis.

Bacterial strains of Shigella dysenteriae I (3818-T and 3818-O) and Shigella enterotoxin altered myoelectric activity of the small intestine in New Zealand White rabbits. These agents were compared with activity caused by sterile culture broth or sterile saline. The altered myoelectric activity was characterized by two distinct complexes: repetitive bursts of action potentials (RBAP), characteristic of invasive strains of bacteria, and the migrating action potential complex (MAPC), characteristic of noninvasive bacteria. RBAP activity was the predominant myoelectric complex observed with S. dysenteriae strain 3818-T, an invader and toxin producer; S. dysenteriae strain 3818-O, a noninvader and toxin producer; and by Shigella enterotoxin. MAPC activity was present but was significantly less in all cases. These studies of the small intestine demonstrate an alteration in myoelectric activity characterized principally by RBAP activity indicative of invasion.

Action Potentials↗

PubMed1981

Organic acid proton donors decrease intestinal secretion caused by enterotoxins.

The effects of several weak acids on the secretory actions of cholera toxin and the heat-stable enterotoxin of Escherichia coli (ST) have been examined in ligated jejunal loops in weanling pigs. Ascorbic and acetic acids had no effect, but L-lactic acid reduced the net fluid secretion caused by cholera toxin. Glutaric acid and p-aminobenzoic acid blocked net fluid secretion caused by cholera toxin or by ST. Antisecretory effects were pH dependent for p-aminobenzoic acid in this study and for nicotinic acid in a previous report (6). At a pH of 5.0, p-aminobenzoic acid treatment increased lumen-to-blood sodium flux and decreased the blood-to-lumen sodium flux caused by cholera toxin. These weak acid effects were more marked on fluid fluxes in enterotoxin-treated loops than in control loops and persisted for 20-30 min after acid removal from loops. These findings are discussed in terms of requirements for antisecretory activity and possible modes of action of antisecretory compounds.

Animals↗

PubMed1997

Hypothalamic-pituitary-adrenal activation by the bacterial superantigen staphylococcal enterotoxin B: role of macrophages and T cells.

Staphylococcal enterotoxin B (SEB) is a bacterial superantigen which stimulates T cells bearing the V beta 8 motif on the T-cell receptor. This stimulation is MHC class II dependent, and in vivo results in a rapid and pronounced T-cell cytokine response. Based on previous evidence that SEB stimulates corticosterone production in BALB/c mice, which possess a high percentage of V beta 8+ T cells, we explored the effects of SEB on the hypothalamic-pituitary-adrenal (HPA) axis and identified the peripheral immunologic cellular requirements for these effects. Administration of SEB stimulates corticosterone in a dose-dependent manner, with peak production of corticosterone occurring by 2 h after intraperitoneal challenge with 50 micrograms SEB. Challenge with staphylococcal enterotoxin A, which activates V beta 3+ and V beta 11+ T cells (deleted during ontogenesis in BALB/c mice), did not increase ACTH or corticosterone production. Furthermore, SEB challenge increased plasma ACTH, which accounted for the increased plasma corticosterone, and increased the expression of c-fos in the PVN region of the hypothalamus. In vivo elimination of macrophages did not prevent the corticosterone response to SEB, suggesting that pituitary-adrenal activation does not require macrophages. However, when mice were pretreated with the T-cell immunosuppressant cyclosporin A, the significantly increased ACTH and corticosterone production in response to SEB was dramatically attenuated. These results demonstrate that bacterial superantigens can stimulate the HPA axis, and that functional T cells may play an obligatory role in this effect.

Adrenal Glands↗

PubMed1973

Development of intestinal adenyl cyclase and its response to cholera enterotoxin.

Adenyl cyclase activity in intestinal membranes has been studied during development in the rabbit fetus from fetal day 17 to 10 days postnatally and in the human fetus from the 10th to the 17th wk of gestation. In the rabbit, the enzyme was already present by fetal day 17 and showed a fourfold peak rise in specific activity by 22 days. By 28 days, the specific activity had fallen toward adult levels and remained constant throughout gestation and the 1st wk of life. Fluoridestimulated activity showed a similar curve, and was 2.5-5 times the basal values. Activities in jejunum and ileum were comparable at all time points studied. Phosphodiesterase activity did not change during gestation. When fetal intestinal segments were incubated in vitro with purified cholera enterotoxin, adenyl cyclase activity in subsequently prepared membranes was increased two- to threefold. This level was not regularly further elevated by fluoride ion. Lithium ion inhibited both the basal and fluoride-stimulated enzyme activity in membranes prepared from rabbit fetuses at term. Lactase activity (reflecting the development of the microvilli) in either whole intestinal homogenates or in the membrane fractions showed a differnet pattern of development, with a rise beginning on fetal day 24 and a plateau just after birth. In intestinal membranes prepared from human fetuses, the activity of both basal and fluoride-stimulated adenyl cyclase tripled from the 10th to the 17th wk of gestation. The data both in the rabbit and in man show that intestinal adenyl cyclase is capable of responding to cholera enterotoxin quite early in gestation. In the rabbit, this occurs before the time of appearance or ville or of an enzyme marker (lactase) for microville. The results support the concept that adenyl cyclase is present in plasma membrane other than the brush border.

Adenylyl Cyclases↗

PubMed1976

Intestinal myoelectric activity in response to live Vibrio cholerae and cholera enterotoxin.

The myoelectric response of the rabbit ileum was studied in response to live Vibrio cholerae culture, a whole cell lysate of cholera, and the purified enterotoxin. Each cholera preparation produced a series of highly organized migrating action potential complexes (MAPC). An MAPC was defined as action potential discharge with a duration of 2.5 s or longer, followed by similar activity on at least one other consecutive electrode site. The mean and modal onset time of MAPC activity occurred 4 h after the infection with live Vibrio cholerae culture, the freeze-dried whole cell lysate preparation, or the purified enterotoxin. After the onset of activity this pattern persisted for the duration of the recording period (up to 12 h). The MAPC had a mean propagation velocity of 0.85+/-0.07 cm/s (mean+/-SEM), which remained constant with time. Direct visual observation of the loop revealed that the MAPC's resulted in contractions that propelled intraluminal contents in an aborad direction. The mean fluid output from the 12-cm ileal loops was 6.4+/-1.1 ml/h (mean+/-SEM). Control experiments consisted of recordings from: (a) a ligated ileal loop into which nothing was placed; (b) a ligated ileal loop into which either uninfected culture broth or 0.9% NaCl solution was injected; (c) a ligated ileal loop infused with 0.9% NaCl solution at a rate of 11.2 ml/h, and (d) rapid injection of 1.0, 2.5, 5.0, or 10.0-ml boluses of 0.9% NaCl into the proximal catheter. MAPC activity was not observed in any of the control experiments. These studies indicate that in addition to a secretory component to cholera, there exists a highly organized MAPC that results in contractions that propel intraluminal contents in an aborad direction.

Action Potentials↗

PubMed1993

A novel superantigen isolated from pathogenic strains of Streptococcus pyogenes with aminoterminal homology to staphylococcal enterotoxins B and C.

Streptococcus pyogenes (group A Streptococcus) has re-emerged in recent years as a cause of severe human disease. Because extracellular products are involved in streptococcal pathogenesis, we explored the possibility that a disease isolate expresses an uncharacterized superantigen. We screened culture supernatants for superantigen activity with a major histocompatibility complex class II-dependent T cell proliferation assay. Initial fractionation with red dye A chromatography indicated production of a class II-dependent T cell mitogen by a toxic shock-like syndrome (TSLS) strain. The amino terminus of the purified streptococcal superantigen was more homologous to the amino termini of staphylococcal enterotoxins B, C1, and C3 (SEB, SEC1, and SEC3), than to those of pyrogenic exotoxins A, B, C or other streptococcal toxins. The molecule, designated SSA, had the same pattern of class II isotype usage as SEB in T cell proliferation assays. However, it differed in its pattern of human T cell activation, as measured by quantitative polymerase chain reaction with V beta-specific primers. SSA activated human T cells that express V beta 1, 3, 15 with a minor increase of V beta 5.2-bearing cells, whereas SEB activated V beta 3, 12, 15, and 17-bearing T cells. Immunoblot analysis of 75 disease isolates from several localities detected SSA production only in group A streptococci, and found that SSA is apparently confined to only three clonal lineages as defined by multilocus enzyme electrophoresis typing. Isolates of one of these lineages, (electrophoretic type 2) are strongly associated with TSLS. The data identify SSA as a novel streptococcal superantigen that appears to be more related structurally to staphylococcal enterotoxins than to streptococcal exotoxins. Because abundant SSA production is apparently confined to only three streptococcal clonal lineages, the data also suggest that the SSA gene has only recently been acquired by S. pyogenes.

Amino Acid Sequence↗

PubMedDate not supplied

Potentiation of inhaled staphylococcal enterotoxin B-induced toxicity by lipopolysaccharide in mice.

Nonhuman primates are the established model for evaluating toxic responses to staphylococcal enterotoxins (SEs), as they react similarly to humans. Rodents are generally considered unresponsive to SEs. Binding affinities and T-cell reactivity suggest that SE binds more efficiently to primate major histocompatability complex class II receptors than to mouse receptors. We investigated the potentiation of staphylococcal enterotoxin B (SEB) inhalation toxicity by lipopolysaccharide (LPS) in BALB/c mice. Lethality occurred only when SEB was potentiated by LPS. Neither SEB nor LPS produced lethal effects alone. Temporal responses of interleukin 1 alpha, tumor necrosis factor alpha, interleukin 2, and interferon-gamma evoked by inhaled SEB were enhanced by LPS. By 24 hr after intoxication, serum cytokines decreased to baseline levels, and consistent pulmonary perivascular leukocytic infiltrates were evident histologically. Histologic lesions induced by inhalation exposure to SEB by mice, with or without potentiation by LPS, were similar to those in the rhesus monkey. Predominant pulmonary lesions included severe, diffuse interstitial and alveolar pulmonary edema, leukocytic infiltrates, mild perivascular edema, and alveolar fibrin deposition. Although the mechanism of aerosolized SEB-induced toxicity has not been completely resolved, similarities in histologic lesions, cytokine responses, and acute dose-response suggest the LPS-potentiated mouse model may be a credible alternative to the nonhuman primate model.

Animals↗

PubMed1984

Entrance of cholera enterotoxin subunits into thymus cells.

Analysis of the staining of cholera enterotoxin on the surface of cells with specific antibodies against each subunit of cholera enterotoxin, using a fluorescence-activated cell sorter and electron microscopy, showed that not only subunit A but also subunit B penetrates the cell membrane. The detection of subunits inside the cell was facilitated by the use of saponin, an agent that increases membrane permeability.

Animals↗

PubMed2006

Staphylococcus aureus enterotoxins induce IL-8 secretion by human nasal epithelial cells.

BACKGROUND: Staphylococcus aureus produces a set of proteins which act both as superantigens and toxins. Although their mode of action as superantigens is well understood, little is known about their effects on airway epithelial cells. METHODS: To investigate this problem, primary nasal epithelial cells derived from normal and asthmatic subjects were stimulated with staphylococcal enterotoxin A and B (SEA and SEB) and secreted (supernatants) and cell-associated (cell lysates) IL-8, TNF-alpha, RANTES and eotaxin were determined by specific ELISAs. RESULTS: Non-toxic concentrations of SEA and SEB (0.01 microg/ml and 1.0 microg/ml) induced IL-8 secretion after 24 h of culture. Pre-treatment of the cells with IFN-gamma (50 IU/ml) resulted in a further increase of IL-8 secretion. In cells from healthy donors pretreated with IFN-gamma, SEA at 1.0 mug/ml induced release of 1009 pg/ml IL-8 (733.0-1216 pg/ml, median (range)) while in cells from asthmatic donors the same treatment induced significantly higher IL-8 secretion - 1550 pg/ml (1168.0-2000.0 pg/ml p = 0.04). Normal cells pre-treated with IFN-gamma and then cultured with SEB at 1.0 mug/ml released 904.6 pg/ml IL-8 (666.5-1169.0 pg/ml). Cells from asthmatics treated in the same way produced significantly higher amounts of IL-8--1665.0 pg/ml (1168.0-2000.0 pg/ml, p = 0.01). Blocking antibodies to MHC class II molecules added to cultures stimulated with SEA and SEB, reduced IL-8 secretion by about 40% in IFN-gamma unstimulated cultures and 75% in IFN-gamma stimulated cultures. No secretion of TNF-alpha, RANTES and eotaxin was noted. CONCLUSION: Staphylococcal enterotoxins may have a role in the pathogenesis of asthma.

Adult↗

PubMed1989

Characteristics and mechanism of action of a heat-stable enterotoxin produced by Klebsiella pneumoniae from infants with secretory diarrhea.

Escherichia coli heat-stable enterotoxins (ST) are classified into STa and STb according to their physicochemical and biologic characteristics. STa induces diarrhea, activating the guanylate cyclase-cGMP system. ST-like enterotoxins can be produced by bacteria other than E. coli, including Klebsiella pneumoniae. A Klebsiella ST has previously been shown to share some chemical and immunologic characteristics with E. coli ST. Aiming to define better the nature of Klebsiella ST, we have screened 237 children with diarrhea and 179 controls for ST-producing Klebsiella, using the SMA. We detected 26 Klebsiella strains from patients, two of which were positive in the SMA, and 36 from controls, all negative for ST. A partial purification was performed using an acetone precipitation followed by ultrafiltration and gel filtration techniques. Klebsiella toxin was heat-stable, methanol-soluble, sensitive to mercaptoethanol, active at acid pH values, but not at pH greater than 8. The time course of Klebsiella toxin in the SMA resembled that of E. coli STa. Klebsiella ST caused reduced Na absorption and net Cl secretion in rabbit ileal mucosa mounted in Ussing chambers. It was found to increase the cGMP but not the cAMP concentration. Finally, Klebsiella ST did not react with anti-E. coli STa MAb in a competitive ELISA. We conclude that K. pneumoniae may induce diarrhea through the production of an STa similar but not identical to E. coli STa.

Bacterial Toxins↗

PubMed1994

Proliferative and cytokine responses by human newborn T cells stimulated with staphylococcal enterotoxin B.

Staphylococcal enterotoxins are potentially valuable tools for investigating the development of T-cell responses because in experimental animals they can elicit either T-cell activation and proliferation or tolerance. Previous studies indicate that human T cells bearing the CD45RA phenotype (which account for the majority of newborn T cells) respond poorly to stimulation by staphylococcal enterotoxin B (SEB) compared with mature T cells from adult blood. The present studies show that the mean frequency of newborn T cells that proliferated in limiting dilution cultures stimulated by SEB was 1:3135, with a 1SD range of 3153-4191 compared with a mean of 1:493 and range of 120-1737 for adult T cells. Neither indomethacin nor the nitric oxide synthesis inhibitor, n-arginine methyl ester, increased SEB responses by newborn cells, arguing against down-regulation of the newborn response by prostaglandin or nitric oxide. Naive (CD45RA+) T cells from adult blood had a responder cell frequency to SEB similar to that of the newborn cells. IL-2 production by newborn cells was delayed compared with adult cells but was equivalent after 3 d of culture. Production of gamma-interferon and IL-4 was greater by adult than newborn cells. Our results indicate that a subset of CD45RA+ cells that is activated by SEB can mature to make IL-4 or gamma-interferon after 3-5 d. The limiting dilution assay results provide a quantitative basis for proliferation by naive T cells against which responses by T cells from healthy and premature newborns can be compared.

Adult↗