The G.U.T. of gut

Bjarnason, Ingvar; Takeuchi, Ken; Bjarnason, Alexander; Adler, Samuel N.; Teahon, K

doi:10.1080/00365520410003326

Cited by 37 publications

(22 citation statements)

References 111 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, the time-dependently increased intestinal permeability for PEG 4000 after the 2 days of ingestion of NSAID in healthy subjects and in particular in IBS patients should be ascribed to NSAID-induced changes in mucosal factors such as putative changes in tight junctions or an altered composition of the mucous surface layer [17.] NSAIDs can reduce the surface hydrophobicity of the gastrointestinal mucosal barrier facilitating exogenous water-dissolved agents to permeate the mucous barrier and damage the underlying epithelium [46,47]. NSAIDs also intracellularly uncouple mitochondrial oxidative phosphorylation, which will contribute to disruption of the integrity of the tight junctions [48,49].…”

Section: Discussionmentioning

confidence: 99%

Intestinal Permeability in Irritable Bowel Syndrome Patients: Effects of NSAIDs

et al. 2009

View full text Add to dashboard Cite

Intestinal permeability and the effect of NSAIDs on permeability were investigated in 14 irritable bowel syndrome (IBS) patients and 15 healthy subjects. In the study, 24-h urinary recoveries of orally administered polyethylene glycols (PEGs 400, 1500, and 4000) were not significantly different in healthy subjects and IBS patients before or after NSAID ingestion. Lactulose mannitol ratios in healthy subjects and IBS patients were not significantly different. Only time-dependent monitoring of PEG excretion showed that NSAIDs enhanced intestinal permeability for PEG 4000 in healthy subjects (P = 0.050) and for PEGs 400, 1500, and 4000 in IBS patients (P = 0.012, P = 0.041, and P = 0.012, respectively). These results show that intestinal permeability in IBS patients is not different from that in healthy subjects; NSAIDs compromise intestinal permeability in IBS patients to a greater extent than in healthy subjects, which suggests that IBS is associated with an altered response of the intestinal barrier to noxious agents.

show abstract

Section: Discussionmentioning

confidence: 99%

Intestinal Permeability in Irritable Bowel Syndrome Patients: Effects of NSAIDs

et al. 2009

View full text Add to dashboard Cite

show abstract

“…An even greater decrease in permeability was observed in CF mice given exogenous IAP, and these mice also had a greater than 80% reduction in small intestinal bacterial overgrowth. Impaired intestinal permeability appears to be a ubiquitous feature of intestinal dysfunction and it occurs even with mild inflammation (54). Additionally, increased permeability is a common feature of microbial dysbiosis.…”

Section: Discussionmentioning

confidence: 99%

Impaired Mucosal Barrier Function in the Small Intestine of the Cystic Fibrosis Mouse

Lisle

Mueller

Boyd

2011

J. pediatr. gastroenterol. nutr.

View full text Add to dashboard Cite

Objectives The intestinal mucosal barrier is important to protect the body from the large numbers of microbes that inhabit the intestines and the molecules they release. Intestinal barrier function is impaired in humans with cystic fibrosis (CF), including reduced activity of the lipopolysaccharide detoxifying enzyme intestinal alkaline phosphatase (IAP) and increased permeability. The objective of this study was to determine the suitability of using the CF mouse to investigate intestinal barrier function, and whether interventions that are beneficial for the CF mouse intestinal phenotype (antibiotics or laxative) would improve barrier function. Also tested were the effects of exogenous IAP administration. Methods The Cftrtm1UNC mouse was used. IAP expression (encoded by the murine Akp3 gene) was measured by qRT-PCR and enzyme activity. Intestinal permeability was assessed by measuring rhodamine dextran plasma levels following gavage. Results CF mice had 40% Akp3 mRNA expression and 30% IAP enzyme activity, as compared to wild type mice. Oral antibiotics and laxative treatments normalized Akp3 expression and IAP enzyme activity in the CF intestine. CF mice had a 5-fold greater transfer of rhodamine dextran from gut lumen to blood. Antibiotic and laxative treatments reduced intestinal permeability in CF mice. Administration of exogenous purified IAP to CF mice reduced intestinal permeability to WT levels and also reduced small intestinal bacterial overgrowth by more than 80%. Conclusions The CF mouse intestine has impaired mucosal barrier function, similar to human CF. Interventions that improve other aspects of the CF intestinal phenotype (antibiotics and laxative) also increased IAP activity and decreased intestinal permeability in CF mice. Exogenous IAP improved permeability and strongly reduced bacterial overgrowth in CF mice, suggesting this may be a useful therapy for CF.

show abstract

“…Indeed, there are more than 30 situations whereby intestinal permeability is increased, and this increase is always followed by an infl ammatory reaction (enteropathy). 29 These enteropathies cannot be easily distinguished from each other macroscopically, suggesting that this effect (i.e., increased intestinal permeability leading to infl ammation) is a common fi nal pathway for a number of small bowel diseases. In NSAID-induced damage to the small bowel, it is increasingly evident that bacteria and their degradation products are the main neutrophil chemoattractants, 21,30,31 and it is of course the neutrophils that defi ne the infl ammation.…”

Section: The Intestinal Barrier Functionmentioning

confidence: 99%

Intestinal permeability in the pathogenesis of NSAID-induced enteropathy

Bjarnason

Takeuchi²

2009

J Gastroenterol

136

View full text Add to dashboard Cite

NSAID enteropathy is associated with significant morbidity and occasionally mortality. There are no proven effective ways of preventing this damage. Because increased intestinal permeability appears to be a central mechanism in the pathogenesis of NSAID enteropathy, it becomes a potential therapeutic target for prevention. At present there are a number of ways to limit the increased permeability, but additional studies are required to assess if this approach reduces the prevalence and severity of NSAID enteropathy.

show abstract

The G.U.T. of gut

Cited by 37 publications

References 111 publications

Intestinal Permeability in Irritable Bowel Syndrome Patients: Effects of NSAIDs

Intestinal Permeability in Irritable Bowel Syndrome Patients: Effects of NSAIDs

Impaired Mucosal Barrier Function in the Small Intestine of the Cystic Fibrosis Mouse

Intestinal permeability in the pathogenesis of NSAID-induced enteropathy

Contact Info

Product

Resources

About