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S C Bischoff

Publications and source records attributed to S C Bischoff.

At least 19 recordsLinked to original sources
PubMed2006

[Therapeutic possibilities of probiotics in antibiotic-related diarrhea].

One of the major problems associated with the use of antibiotics is the occurrence of antibiotic-related diarrhea. Although most such cases of diarrhea are harmless, in individual cases it may lead on to fulminant colitis. In 10-20% of the patients, the causal factor is infection with Clostridium difficile, which multiplies unhindered in patients on antibiotics. In the meantime, controlled, randomized studies have shown that probiotics can exercise a preventive effect in antibiotic-related diarrhea. The administration of Saccharomyces boulardii or Lactobacillus rhamnosus GG reduces the relative risk of an antibiotic-related diarrhea developing by 0.5. The data are more uniform in children than in adults.

Adult↗
PubMed2006

Repeated administration of a vitamin preparation containing glycocholic acid in patients with hepatobiliary disease.

BACKGROUND: Until now, hydrophilic and lipophilic vitamin preparations had to be administered separately during total parenteral nutrition. By addition of glycocholic acid, a vitamin supplement (Cernevit, Baxter, Heidelberg, Germany) was developed that combines all vitamins into one vial. However, little information exists about possible consequences of bile acid administration such as glycocholic acid, especially if liver disease is pre-existing. AIM: To evaluate the effects of total parenteral nutrition with a vitamin preparation containing high doses of glycocholic acid in patients with and without liver disease. METHODS: In a prospective, randomized-controlled trial, 74 patients, 36 of them with hepatobiliary disease, received total parenteral nutrition for 16 +/- 11 days, either with Cernevit or control vitamin supplements. Patients were closely monitored for clinical and biochemical parameters including serum bile acid profiles measured by high-performance liquid chromatography. RESULTS: Serum glycocholic acid increased in patients with liver disease treated with Cernevit, whereas total bile acids did not significantly change. Other liver function tests remained stable during treatment. No adverse events during Cernevit administration were noted except for a reversible slight increase of transaminases in one patient. CONCLUSIONS: Cernevit was well tolerated after repeated dosing, even in patients with severe liver disease. Apart from standard controls of liver biochemistry, no specific surveillance is necessary during treatment with Cernevit.

Adult↗
PubMed2006

Evaluation of colonoscopic allergen provocation as a diagnostic tool in dogs with proven food hypersensitivity reactions.

OBJECTIVE: To evaluate the colonoscopic allergen provocation (COLAP) test as a new tool for the diagnosis of IgE-mediated food allergy. METHODS: Oral food challenges as well as COLAP testing were performed in a colony of nine research dogs with proven immediate-type food allergic reactions. In addition, COLAP was performed in five healthy dogs. RESULTS: When compared with the oral challenge test, COLAP accurately determined 18 of 23 (73 per cent) positive oral challenge reactions (73 per cent) in dogs with food allergies and was negative in the healthy dogs. CLINICAL SIGNIFICANCE: The accuracy of this new test may be higher than that for gastric sensitivity testing. Therefore, COLAP holds promise as a new test to confirm the diagnosis of suspect IgE-mediated food allergy in dogs.

Allergens↗
PubMed2005

Selective expression of histamine receptors H1R, H2R, and H4R, but not H3R, in the human intestinal tract.

BACKGROUND AND AIMS: Histamine is known as a regulator of gastrointestinal functions, such as gastric acid production, intestinal motility, and mucosal ion secretion. Most of this knowledge has been obtained from animal studies. In contrast, in humans, expression and distribution of histamine receptors (HR) within the human gastrointestinal tract are unclear. METHODS: We analysed HR expression in human gastrointestinal tissue specimens by quantitative reverse transcription-polymerase chain reaction and immunostaining. RESULTS: We found that H1R, H2R, and H4R mRNA were expressed throughout the gastrointestinal tract, while H3R mRNA was absent. No significant differences in the distribution of HR were found between different anatomical sites (duodenum, ileum, colon, sigma, and rectum). Immunostaining of neurones and nerve fibres revealed that H3R was absent in the human enteric nervous system; however, H1R and H2R were found on ganglion cells of the myenteric plexus. Epithelial cells also expressed H1R, H2R and, to some extent, H4R. Intestinal fibroblasts exclusively expressed H1R while the muscular layers of human intestine stained positive for both H1R and H2R. Immune cells expressed mRNA and protein for H1R, H2R, and low levels of H4R. Analysis of endoscopic biopsies from patients with food allergy and irritable bowel syndrome revealed significantly elevated H1R and H2R mRNA levels compared with controls. CONCLUSIONS: We have demonstrated that H1R, H2R and, to some extent, H4R, are expressed in the human gastrointestinal tract, while H3R is absent, and we found that HR expression was altered in patients with gastrointestinal diseases.

Cells, Cultured↗
PubMed2005

Glutamine-enriched total parenteral nutrition in patients with inflammatory bowel disease.

BACKGROUND: Studies in animal models of inflammatory bowel disease (IBD) suggest that supplementation of total parenteral nutrition with glutamine (gln), a conditionally essential amino acid in catabolic conditions, increases gln plasma concentrations, reduces intestinal damage, improves nitrogen balance and may improve the course of the disease. However, human data supporting this assumption are missing. METHODS: A total of 24 consecutive patients with an acute exacerbation of IBD (19 Crohn's disease; five ulcerative colitis) and scheduled for total parenteral nutrition (TPN) (>7 days) were randomised. Parallel to a standardised anti-inflammatory therapy, the patients received either a TPN with 1.5 g/kg body weight of a standard amino acid or an isonitrogenic, isocaloric TPN with 1.2 g/kg body weight of a standard amino acid and 0.3 g/kg L-alanine-L-glutamine. Primary end points were gln plasma concentrations and intestinal permeability assessed by urinary lactulose and D-xylose ratio. RESULTS: Gln plasma levels did not differ significantly in either group throughout the study. Intestinal permeability did not change within 7 days either with or without gln supplementation (Delta-lactulose/xylose ratio: 0.01+/-0.05 (gln+) vs 0.02+/-0.1 (gln-)). The observed changes in inflammatory and nutritional parameters, and also disease activity, length of TPN and hospital stay, were independent of glutamine substitution. Five (41%) patients in the gln+ group and three (25%) patients in the gln- group needed surgical intervention. CONCLUSION: Although limited by the sample size, these results do not support the hypothesis that glutamine substitution has an obvious biochemical or clinical benefit in patients with active IBD scheduled for total parenteral nutrition.

Acute Disease↗
PubMed2005

Development of an in vitro system for the study of allergens and allergen-specific immunoglobulin E and immunoglobulin G: Fcepsilon receptor I supercross-linking is a possible new mechanism of immunoglobulin G-dependent enhancement of type I allergic reactions.

BACKGROUND: IgE-dependent activation of mast cells (MCs) is a key pathomechanism of type I allergies. In contrast, allergen-specific IgG Abs are thought to attenuate immediate allergic reactions by blocking IgE binding and by cross-linking the inhibitory Fcgamma receptor IIB on MCs. OBJECTIVES: To establish a defined in vitro system using human MCs to study the biological activity of allergens and to investigate the role of allergen-specific IgE and IgG. METHODS: Purified human intestinal MCs sensitized with different forms of specific IgE Abs were triggered by monomeric and oligomeric forms of recombinant Bet v 1, the major birch pollen allergen, in the presence or absence of allergen-specific IgG Abs. Results MCs sensitized with an anti-Bet v 1 IgE mAb or sera obtained from birch pollen allergic patients released histamine and sulphidoleukotrienes after exposure to oligomeric Bet v 1. Monomeric Bet v 1 provoked mediator release only in MCs sensitized with patients sera but not in MCs sensitized with anti-Bet v 1 IgE mAb. Interestingly, MC activation could be induced by supercross-linking of monomeric Bet v 1 bound to monovalent IgE on MCs with a secondary allergen-specific IgG pAb. By using IgG F(ab')2 fragments we provide evidence that this effect is not a result of IgG binding to Fcgamma receptors. CONCLUSION: This assay represents a new tool for the in vitro study of MC activation in response to natural and genetically modified allergens. Fcepsilon receptor I supercross-linking by allergen-specific IgG Abs provides a possible new mechanism of IgG-dependent enhancement of type I allergic reactions.

Allergens↗
PubMed2005

Human mast cell mediator cocktail excites neurons in human and guinea-pig enteric nervous system.

Neuroimmune interactions are an integral part of gut physiology and involved in the pathogenesis of inflammatory and functional bowel disorders. Mast cells and their mediators are important conveyors in the communication from the innate enteric immune system to the enteric nervous system (ENS). However, it is not known whether a mediator cocktail released from activated human mast cells affects neural activity in the ENS. We used the Multi-Site Optical Recording Technique to image single cell activity in guinea-pig and human ENS after application of a mast cell mediator cocktail (MCMC) that was released from isolated human intestinal mucosa mast cells stimulated by IgE-receptor cross-linking. Local application of MCMC onto individual ganglia evoked an excitatory response consisting of action potential discharge. This excitatory response occurred in 31%, 38% or 11% neurons of guinea-pig submucous plexus, human submucous plexus, or guinea-pig myenteric plexus, respectively. Compound action potentials from nerve fibres or fast excitatory synaptic inputs were not affected by MCMC. This study demonstrates immunoneural signalling in the human gut and revealed for the first time that an MCMC released from stimulated human intestinal mast cells induces excitatory actions in the human and guinea-pig ENS.

Animals↗
PubMed2005

Epsilon germ-line and IL-4 transcripts are expressed in human intestinal mucosa and enhanced in patients with food allergy.

BACKGROUND: The mechanisms of gastrointestinal (GI) food allergy (FA) are poorly understood. Immunoglobulin E (IgE) is increased in stools from patients with FA, as well as the number of cells carrying IgE in intestinal mucosa, but the origin of IgE production remains unknown. To investigate a local production of IgE in intestine, we analysed the levels of transcripts for epsilon germ-line (epsilonGT), and potential regulators of IgE production, IL-4, IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha in intestinal mucosa of adult patients with FA. METHODS: Endoscopic biopsies were obtained from the caecum of 25 patients with FA and 14 control patients. The levels of epsilonGT, IL-4, IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha mRNA were analysed by real-time RT-PCR and compared with unpaired nonparametric Mann-Whitney test. RESULTS: The mean epsilonGT transcript level in caecum was increased in FA patients compared with control patients (P < 0.05). IL-4 mRNA expression was also increased in FA patients (P < 0.05), whereas mRNA expression for IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha mRNA expression was not altered. However, the ratio of IL-4 mRNA/IFN-gamma mRNA was significantly increased in FA patients (P < 0.05). No correlation was observed between epsilonGT transcripts expression in intestinal mucosa and total IgE levels in serum. CONCLUSIONS: This study shows that (i) epsilonGT transcripts are expressed in human intestinal mucosa; (ii) epsilonGT and IL-4 transcripts are increased in caecal mucosa from patients with FA. These results suggest local production of IgE in intestine that might be of importance for inflammatory reactions in the GI tract.

Adult↗
PubMed2005

Growth, phenotype, and function of human intestinal mast cells are tightly regulated by transforming growth factor beta1.

BACKGROUND AND AIMS: Transforming growth factor beta1 (TGF-beta1) is expressed in the healthy human intestine and controls mucosal immune responses and inflammation by regulating the function of lymphocytes, macrophages, dendritic cells, and eosinophils. Here, we asked whether human intestinal mast cells (MC) might also be subject to immunoregulation by TGF-beta1. METHODS: MC were isolated from the intestinal mucosa, purified, and cultured in vitro in the presence of stem cell factor (SCF) with or without TGF-beta1. Growth characteristics, phenotype, and immunological mediator release of MC were analysed by reverse transcription-polymerase chain reaction, flow cytometry, immunocytochemistry, western blot, and different immunoassays, respectively. RESULTS: TGF-beta1 dose dependently (ED50 approximately = 0.1 ng/ml) inhibited SCF dependent growth of human intestinal MC by both enhancing apoptosis and decreasing proliferation. In parallel, TGF-beta1 increased the percentage of connective tissue-type MC expressing tryptase and chymase while downregulating expression of the receptors for IgE and SCF. Furthermore, TGF-beta1 dramatically changed the profile of mediators released by MC following IgE receptor crosslinking. Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1. CONCLUSIONS: Our data indicate that TGF-beta1 acts as a novel potent inhibitor and modulator of human intestinal MC effector functions. The change in MC mediator release profile and protease expression induced by TGF-beta1 might be of relevance for the control of MC associated disorders of the intestine such as allergic reactions, Crohn's disease, irritable bowel syndrome, and parasitic infection.

Apoptosis↗
PubMed2004

Mast cells and eosinophils have a potential profibrogenic role in Crohn disease.

BACKGROUND: Mast cells and eosinophils have an important role in allergic inflammation and probably also in chronic inflammatory diseases resulting in fibrosis, such as Crohn disease where fibrosis is present as strictures. The involvement of mast cells and eosinophils in Crohn disease fibrosis was investigated. METHODS: Biopsies from diseased foci were stained for mast cells, eosinophils, anti-collagen type IV and VIII, laminin and alpha-smooth muscle actin (alpha-SMA) (IHC). Fibroblasts outgrown from the biopsies and a normal fetal intestinal fibroblast line were cultured in the presence of the human mast cell line HMC-1, or of human peripheral blood eosinophil (MACS, purity > 98%) sonicates, or of selected mediators. Fibroblast proliferation (3H-thymidine), collagen synthesis ([3H]-proline) and collagen gel contraction were evaluated. RESULTS: Mast cells were present in all the biopsies and only faintly positive for extra cellular matrix (ECM) products. Pronounced eosinophilia was detected in only two cases. Mast cell sonicates increased both Crohn disease (alpha-SMA positive) and control fibroblast proliferation, decreased collagen production and increased collagen gel contraction. Eosinophil sonicates increased fibroblast proliferation, gel contraction and collagen production. TNF-alpha decreased collagen production. Histamine, tryptase and chymase had no influence. CONCLUSIONS: These in vitro data show that mast cells and eosinophils could be involved in modulating Crohn disease fibrosis by directly influencing intestinal fibroblast properties.

Cell Communication↗
PubMed2004

Substance P and other neuropeptides do not induce mediator release in isolated human intestinal mast cells.

Neuropeptides such as substance P (SP) and related peptides are supposed to act as mast cell agonists, and thus as mediators of neuroimmune interactions. The data supporting this hypothesis were obtained mostly from rodent experiments. Here, we studied for the first time the effect of SP and other peptides on mediator release in human intestinal mast cells, either unpurified or enriched to 85-99% purity. We found that SP at 0.1-100 micromol L(-1), or other peptides including neurokinin A and B, calcitonin gene-related peptide, vasoactive intestinal peptide and serotonin at 1 micromol L(-1) do not induce release of mediators such as histamine, sulphidoleukotrienes, and tumour necrosis factor alpha. The peptides also failed to cause mediator release in mast cells isolated from inflamed tissue derived from Crohn's disease. Using reverse transcriptase-polymerase chain reaction, flow cytometry and immunohistochemistry, we could show that human intestinal mast cells do not express the tachykinin receptors NK-1, NK-2, or NK-3 under basal conditions. However, upon stimulation by immunoglobulin E (IgE) receptor-crosslinking, which induces an extensive mediator release reaction, a subpopulation of mast cells clearly expressed NK-1, the SP receptor. In conclusion, our data show that SP and other neuropeptides do not act as secretagogues in human intestinal mast cells that have not been pre-activated by IgE receptor-crosslinking.

Cells, Cultured↗
PubMed2003

What is the physiological function of mast cells?

Under physiological conditions, skin mast cells preferentially localize around nerves, blood vessels and hair follicles. This observation, which dates back to Paul Ehrlich, intuitively suggests that these enigmatic, multifacetted protagonists of natural immunity are functionally relevant to many more aspects of tissue physiology than just to the generation of inflammatory and vasodilatory responses to IgE-dependent environmental antigens. And yet, for decades, mainstream-mast cell research has been dominated by a focus on the -undisputedly prominent and important - mast cell functions in type I immune responses and in the pathogenesis and management of allergic diseases. Certainly, it is hard to believe that the very large and rather selectively distributed number of mast cells in normal, uninflamed, non-infected, non-traumatized mammalian skin or mucosal tissue simply hanging around there lazily day and night, just wait for the odd allergen or parasite-associated antigen to come by so the mast cell can finally swing into action. Indeed, the past decade has witnessed a renaissance of mast cell research 'beyond allergy', along with a more systematic exploration of the surprisingly wide range of physiological functions that mast cells may be involved in. The current debate sketches many exciting horizons that have recently come into our vision during this intriguing, ongoing search.

Animals↗
PubMed2002

Mast cells involvement in the inflammation and fibrosis development of the TNBS-induced rat model of colitis.

BACKGROUND: Mast cells have been implicated in chronic inflammatory conditions resulting in fibrosis, such as Crohn disease. However, a link between inflammation, fibrosis and mast cells has not been demonstrated in human or animal intestinal diseases. This work was undertaken to analyze whether mast cells play a role in inflammation and fibrosis in the TNBS-induced rat colitis. METHODS: Rats were rectally instilled 2,4,6,-trinitrobenzene sulfonic acid in ethanol, and immediately or 4 days later injected daily i.p. with nedocromil sodium, a mast cell stabilizer, compound 48/80, a mast cell activator, or saline. Rats were sacrificed 5 days post-TNBS, or on day 21. Intestinal inflammation and fibrosis were assessed by gross and histopathological evaluation. Colonic mast cell numbers (toluidine blue) and collagen (type I mRNA expression) were evaluated. Mast cell sonicate was added to rat colon fibroblasts. Fibroblast proliferation (3H-thymidine), collagen synthesis (3H-proline) and contractile activity (tridimensional collagen lattice contraction) were then assessed. RESULTS: Nedocromil reduced inflammation and fibrosis possibly by decreasing mast cell numbers and activation and consequent collagen production. Compound 48/80 slightly enhanced the severity of the disease by activating mast cells. Mast cells increased fibroblast proliferation, collagen production and contractile activity. CONCLUSIONS: Mast cells are involved in the gastrointestinal tract inflammation and fibrosis of the TNBS-colitis rats.

Animals↗