Untitled

Gut Microorganisms and the GI Tract:
The Lastest Research


Microbial Toxins Influence Most Digestive Symptoms

 

Main Menu


Microorganisms Create the Leaky Gut.

Microorganisms has also been found to be associated with leaky gut in both animal and human models. We have assembled a colection of articles about the role of microorganisms and the leaky gut.

View this article in PubMed
1: Scand J Gastroenterol. 1997 Jun;32(6):556-63.

Luminal bacteria and small-intestinal permeability.

* Riordan SM, * McIver CJ, * Thomas DH, * Duncombe VM, * Bolin TD, * Thomas MC.

Dept. of Gastroenterology, Prince of Wales Hospital, Sydney, Australia.

BACKGROUND: The influence of luminal bacteria on small-intestinal permeability has not been fully assessed. This study addressed this issue. METHODS: Thirty-four subjects (mean age 64 years; range 22-95 years) were investigated for possible small-intestinal bacterial overgrowth (SIBO) with culture of a small-intestinal aspirate. A lactulose/mannitol small-intestinal permeability test was performed, small-intestinal histology assessed and serum vitamin B12 concentrations measured in all subjects. Permeability was also assessed in a control group of 34 asymptomatic volunteers. RESULTS: Urinary lactulose/mannitol ratios were significantly increased in subjects with SIBO with colonic-type flora (P < 0.0005), even in the absence of villous atrophy. Urinary lactulose/mannitol ratios were increased in this group due to significantly increased urinary lactulose concentrations (P < 0.0005) rather than reduced urinary mannitol levels, after correcting for inter-subject variations in renal function. Counts of intraepithelial lymphocytes of CD8 phenotype were significantly increased in this group (P = 0.003). Although a significant correlation was found between intraepithelial lymphocyte counts and small-intestinal permeability overall (P < 0.002), these counts were not significantly different in subjects with SIBO with colonic-type flora whose permeability values were < or = > 0.028, the upper limit of normal in asymptomatic controls. Serum vitamin B12 concentrations did not differ significantly between groups (P > 0.5). Ageing did not independently influence small-intestinal permeability (P > 0.5). CONCLUSIONS: Small-intestinal permeability is increased in subjects with SIBO with colonic-type bacteria. This effect is independent of ageing and not mediated by vitamin B12 deficiency. Although counts of intraepithelial lymphocytes of CD8 phenotype are increased in this disorder, it is also unlikely that these cells play an important causative role in this process. Routine light microscopic assessment underestimates the prevalence of small-intestinal functional disturbance in this disorder.

PMID: 9200287 [PubMed - indexed for MEDLINE]


http://www.nlm.nih.gov/medlineplus/ency/article/000224.htm
Campylobacter enteritis is an infection in the small intestine caused by Campylobacter jejuni, a type of bacteria. Patients who developed an acute case of Campylobacter enteritis were compared to people who did not have any digestive symptoms(asymptomatic controls). They had significantly higher levels of gut permeability, as assessed by the lactulose/mannitol ratio. This shows that bacterial infections are capable of increasing the gut permeability.

http://gut.bmj.com/cgi/content/abstract/47/6/804
Gut 2000;47:804-811 ( December )

Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome R C Spillera, D Jenkinsb, J P Thornleyb, J M Hebdena, T Wrighta, M Skinnerb, K R Nealc

a Division of Gastroenterology, University Hospital Nottingham, Nottingham, UK, b Department of Pathology, University Hospital Nottingham, Nottingham, UK, c Department of Public Health Medicine, University Hospital Nottingham, Nottingham, UK

Correspondence to: Dr R C Spiller, Division of Gastroenterology, C Floor, South Block, University Hospital, Nottingham NG7 2UH, UK. robin.spiller@nottingham.ac.uk

Accepted for publication 22 June 2000

BACKGROUND AND AIMS---Post-dysenteric irritable bowel syndrome (PD-IBS) develops in up to 25% of patients following Campylobacter enteritis. Our aim was to define the pathological basis of this subgroup of IBS. METHODS---Twenty one patients (group 1) underwent serial rectal biopsy and gut permeability testing following acute Campylobacter enteritis as did 10 PD-IBS patients (group 2) and 12 asymptomatic controls. RESULTS---In group 1, enteroendocrine cell (EC) numbers were markedly increased initially and at six and 12 weeks (p<0.001) compared with controls. Gut permeability, as assessed by the lactulose/mannitol ratio, was significantly elevated, initially and at 12 weeks (p<0.005). CD3, CD4, and CD8 lymphocyte counts in the lamina propria and intraepithelial lymphocytes (IEL) were significantly increased initially compared with controls. At visit 1, EC numbers were positively correlated with CD3 counts (r=0.6, p=0.01). At one year, seven subjects (five with persistent loose stools) had rectal biopsies which showed significantly elevated EC, CD3, and IEL counts. In group 2, EC and IEL counts were significantly increased compared with controls (p<0.001), as was gut permeability (p<0.01). CONCLUSION---Increased EC, T lymphocytes, and gut permeability are acute changes following Campylobacter enteritis which can persist for more than a year and may contribute to PD-IBS.

Keywords: irritable bowel syndrome; Campylobacter; enteroendocrine cell; T lymphocytes


View this article in PubMed
Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure.

* El Asmar R, * Panigrahi P, * Bamford P, * Berti I, * Not T, * Coppa GV, * Catassi C, * Fasano A.

Department of Pediatrics and Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

BACKGROUND & AIMS: Enteric infections have been implicated in the pathogenesis of both food intolerance and autoimmune diseases secondary to the impairment of the intestinal barrier. On the basis of our recent discovery of zonulin, a modulator of small-intestinal tight junctions, we asked whether microorganisms might induce zonulin secretion and increased small-intestinal permeability. METHODS: Both ex vivo mammalian small intestines and intestinal cell monolayers were exposed to either pathogenic or nonpathogenic enterobacteria. Zonulin production and changes in paracellular permeability were monitored in Ussing chambers and micro-snapwells. Zonula occludens 1 protein redistribution after bacteria colonization was evaluated on cell monolayers. RESULTS: Small intestines exposed to enteric bacteria secreted zonulin. This secretion was independent of either the species of the small intestines or the virulence of the microorganisms tested, occurred only on the luminal aspect of the bacteria-exposed small-intestinal mucosa, and was followed by a decrease in small-intestinal tissue resistance (transepithelial electrical resistance). The transepithelial electrical resistance decrement was secondary to the zonulin-induced tight junction disassembly, as also shown by the disengagement of the protein zonula occludens 1 protein from the tight junctional complex. CONCLUSIONS: This zonulin-driven opening of the paracellular pathway may represent a defensive mechanism, which flushes out microorganisms and contributes to the host response against bacterial colonization of the small intestine.

PMID: 12404235 [PubMed - indexed for MEDLINE]


View this article in PubMed
Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.

* Madsen KL, * Malfair D, * Gray D, * Doyle JS, * Jewell LD, * Fedorak RN.

Department of Medicine, University of Alberta, Edmonton, Canada.

The normal intestinal epithelium provides a barrier relatively impermeable to luminal constituents. However, patients with inflammatory bowel disease experience enhanced intestinal permeability that correlates with the degree of injury. IL-10 gene-deficient mice were studied to determine whether increased intestinal permeability occurs as a primary defect before the onset of mucosal inflammation or is secondary to mucosal injury. At 2 weeks of age, IL-10 gene-deficient mice show an increase in ileal and colonic permeability in the absence of any histological injury. This primary permeability defect is associated with increased mucosal secretion of interferon-gamma and tumor necrosis factor-alpha, and does not involve an increase in nitric oxide synthase activity. Colonic permeability remains elevated as inflammation progresses, while ileal permeability normalizes by 6 weeks of age. IL-10 gene-deficient mice raised under germ-free conditions have no inflammation, and demonstrate normal permeability and cytokine levels. This data suggests that the intestinal permeability defect in IL-10 gene-deficient mice occurs due to a dysregulated immune response to normal enteric microflora and, furthermore, this permeability defect exists prior to the development of mucosal inflammation.

PMID: 10579119 [PubMed - indexed for MEDLINE]


Untitled

This website is under construction.