Nejvíce citovaný článek - PubMed ID 18661294
The intestinal microflora of childhood patients with indicated celiac disease
BACKGROUND AND AIMS: Celiac disease (CD) is a chronic inflammatory disorder of the small intestine that is induced by dietary wheat gluten proteins (gliadins) in genetically predisposed individuals. The overgrowth of potentially pathogenic bacteria and infections has been suggested to contribute to CD pathogenesis. We aimed to study the effects of gliadin and various intestinal bacterial strains on mucosal barrier integrity, gliadin translocation, and cytokine production. METHODOLOGY/PRINCIPAL FINDINGS: Changes in gut mucosa were assessed in the intestinal loops of inbred Wistar-AVN rats that were reared under germ-free conditions in the presence of various intestinal bacteria (enterobacteria and bifidobacteria isolated from CD patients and healthy children, respectively) and CD-triggering agents (gliadin and IFN-γ) by histology, scanning electron microscopy, immunofluorescence, and a rat cytokine antibody array. Adhesion of the bacterial strains to the IEC-6 rat cell line was evaluated in vitro. Gliadin fragments alone or together with the proinflammatory cytokine interferon (IFN)-γ significantly decreased the number of goblet cells in the small intestine; this effect was more pronounced in the presence of Escherichia coli CBL2 and Shigella CBD8. Shigella CBD8 and IFN-γ induced the highest mucin secretion and greatest impairment in tight junctions and, consequently, translocation of gliadin fragments into the lamina propria. Shigella CBD8 and E. coli CBL2 strongly adhered to IEC-6 epithelial cells. The number of goblet cells in small intestine increased by the simultaneous incubation of Bifidobacterium bifidum IATA-ES2 with gliadin, IFN-γ and enterobacteria. B. bifidum IATA-ES2 also enhanced the production of chemotactic factors and inhibitors of metalloproteinases, which can contribute to gut mucosal protection. CONCLUSIONS: Our results suggest that the composition of the intestinal microbiota affects the permeability of the intestinal mucosa and, consequently, could be involved in the early stages of CD pathogenesis.
- MeSH
- Bacteria patogenita MeSH
- bakteriální toxiny farmakologie MeSH
- Bifidobacterium patogenita MeSH
- celiakie etiologie MeSH
- cytokiny biosyntéza MeSH
- Enterobacteriaceae patogenita MeSH
- gliadin farmakokinetika farmakologie MeSH
- gnotobiologické modely MeSH
- interakce hostitele a patogenu účinky léků MeSH
- interferon gama farmakologie MeSH
- krysa rodu Rattus MeSH
- permeabilita MeSH
- pohárkové buňky patologie MeSH
- střeva mikrobiologie patologie MeSH
- střevní sliznice účinky léků metabolismus mikrobiologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- bakteriální toxiny MeSH
- cytokiny MeSH
- gliadin MeSH
- interferon gama MeSH
The "cocktail" of human origin rifampicin-resistant bifidobacteria (RRBs) and RRBs from commercial products was administrated to 9 volunteers aged from 22 to 46 years and the survival ability in gastrointestinal tract of these strains was determined. Bifidobacteria represented 0-8 % of total anaerobes detected in gastrointestinal tract of volunteers before the administration of probiotic strains. After the administration of probiotics, bifidobacterial counts increased to 16 % of total bacterial counts. RRBs formed 9-44 % of total counts of bifidobacteria. Then, the counts of RRBs decreased at day 7 after administration, and they were not detected after 14 d. In our study, suitable probiotic bifidobacterial strains for human should be chosen on the basic of in vitro test but the results showed that no strain was able to colonize human tract permanently.
- MeSH
- Bifidobacterium fyziologie MeSH
- dospělí MeSH
- experimenty na lidech MeSH
- gastrointestinální trakt mikrobiologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikrobiální viabilita * MeSH
- počet mikrobiálních kolonií MeSH
- probiotika aplikace a dávkování MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Intestinal microbiota in exclusively breast-fed infants with blood-streaked stools and in healthy exclusively breast-fed babies was compared. Total anaerobes, bifidobacteria, lactobacilli, coliform bacteria, enterococci and clostridia were quantified by cultivation methods in feces of 17 full-term exclusively breastfed patients (aged 16.3 +/- 7.4 weeks) with blood-streaked stools and in the control group of 22 healthy fullterm exclusively breast-fed infants (13.7 +/- 6.4 weeks). Specific fluorescence in situ hybridization kits for Bifidobacterium spp. were used for the quantitative detection of bifidobacteria in samples. Control samples had significantly (p < 0.05) higher counts of total anaerobes. Bifidobacteria were not detected in patients' samples in 65 % and in controls in 36 % (p < 0.01). Bifidobacteria counts were also significantly higher in the control group (p < 0.01). Furthermore, clostridia strains were detected only in feces from bifidobacteria-negative infants reaching counts >8 log CFU/g. Lactobacilli were not detected in 65 % patients and in 45 % control samples. However, this difference was not significant as well as the difference in lactobacilli counts. Eosinophilia was observed in 35 % of patients, low IgA concentration in 71 % and also low IgG concentration in 71 %. pANCA positivity was found in 53 % of patients. In conclusion a significant low proportion of bifidobacterial microbiota in patients with blood-streaked stools was shown in comparison with controls.
- MeSH
- Bacteria izolace a purifikace MeSH
- feces mikrobiologie MeSH
- imunoglobulin A krev MeSH
- imunoglobulin G krev MeSH
- kojenec MeSH
- kojení * MeSH
- lidé MeSH
- proktokolitida imunologie mikrobiologie MeSH
- střeva mikrobiologie MeSH
- Check Tag
- kojenec MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- imunoglobulin A MeSH
- imunoglobulin G MeSH