Pretreatment but not treatment with probiotics abolishes mouse intestinal barrier dysfunction in acute pancreatitis

Rychter, Jakub; Minnen, L. Paul van; Verheem, André; Timmerman, Harro M.; Rijkers, Ger T.; Schipper, Marguérite E.I.; Gooszen, Hein G.; Akkermans, L.M.A.; Kroese, A.B.A.

doi:10.1016/j.surg.2008.09.011

Cited by 43 publications

(29 citation statements)

References 38 publications

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“…The protective action of probiotics coincided with inhibition of oxidative stress, downregulation of occludin and claudin-1, upregulation of claudin-2, and reduction of mucosal injury. However, treatment at the time of acute pancreatitis induction was ineffective [175]. The probiotic mixture VSL#3 significantly ameliorated the disease activity index and reduced histological signs of inflammation in acute DSS colitis [176].…”

Section: Probiotic Bacteria To Fight Pathogens and Reconstitute A Promentioning

confidence: 99%

“…In a rat model of alcohol-induced steatohepatitis, L. rhamnosus attenuated alcohol-induced loss of intestinal barrier, ameliorated tissue (gut and liver) and systemic oxidative stress, and significantly reduced the severity of the disease, as shown by a decrease in hepatic fat content and signs of inflammation [173]. The probiotic mixture, Probiotics Ecologic ® 641, was also effective as a preventive treatment in a rat model of acute pancreatitis which is associated with severe ileal mucosal barrier dysfunction and translocation of luminal bacteria that cause infectious complications [174,175]. Pretreatment with probiotics antagonized the increase in both paracellular and transcellular permeability and tissue conductance, thus preventing E. coli translocation.…”

Section: Probiotic Bacteria To Fight Pathogens and Reconstitute A Promentioning

confidence: 99%

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Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Catalioto

Maggi²,

Giuliani³

2011

CMC

137

102

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The intestinal epithelial monolayer constitutes a physical and functional barrier between the organism and the external environment. It regulates nutrients absorption, water and ion fluxes, and represents the first defensive barrier against toxins and enteric pathogens. Epithelial cells are linked together at the apical junctional complex by tight junctions that reduce the extracellular space and the passage of charge entities while forming a physical barrier to lipophilic molecules. Cultured intestinal epithelial cells have been extensively used to study intestinal absorption of newly synthesized drugs and the regulation of tight junctions structure and function. In vitro mild irritants, proinflammatory cytokines, toxins and pathogens, and adverse environmental conditions open tight junctions and increase paracellular permeability, an effect often accompanied by immune activation of the enterocytes. Conversely, inhibition of proinflammatory cytokines, exposure to growth factors and probiotics, among others, exert a protective effect. Impaired barrier function results from activation of signalling pathways that lead to alteration of junctional proteins expression and/or distribution. In vivo, intestinal barrier dysfunction is associated with various intestinal and non-intestinal disorders including inflammatory bowel disease, celiac disease, and diarrhoeal infection. This review will describe the current knowledge of the mechanisms regulating tight junctions and intestinal permeability, how these findings have lead to a better understanding of barrier alteration in human intestinal disorders, and what the emerging therapies to treat these pathologies are.

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Section: Probiotic Bacteria To Fight Pathogens and Reconstitute A Promentioning

confidence: 99%

Section: Probiotic Bacteria To Fight Pathogens and Reconstitute A Promentioning

confidence: 99%

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Catalioto

Maggi²,

Giuliani³

2011

CMC

137

102

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show abstract

“…Bacterial colonization of the inflamed pancreas is involved in the latter cases and, in fact, infection of necrotic pancreatic tissue is one of the most important causes of mortality in acute pancreatitis (Frossard et al, 2008). It is now generally accepted that such colonization and associated inflammation result from failure of intestinal barrier function and translocation of intestinal microflora into the splanchnic vascular bed (Frossard et al, 2008; Rychter et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis

et al. 2012

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SUMMARY The intracellular sensor NOD1 has important host defense functions relating to a variety of pathogens. Here we showed that this molecule also participated in the induction of a non-infectious pancreatitis via its response to commensal organisms. Pancreatitis induced by high-dose cerulein (a cholecystokinin receptor agonist) administration depends on NOD1 stimulation by gut microflora. To analyze this NOD1 activity we induced pancreatitis by simultaneous administration of low-dose of cerulein (that does not itself induce pancreatitis) and FK156, an activator of NOD1 that mimics the effect of gut bacteria that have breached the mucosal barrier. The pancreatitis was dependent on acinar cell production of the chemokine MCP-1 and the intra-pancreatic influx of CCR2+ inflammatory cells. Moreover, MCP-1 production involved activation of the transcription factors NF-κB and STAT3, each requiring complementary NOD1 and cerulein signaling. These studies indicate that gut commensals enable non-infectious pancreatic inflammation via NOD1 signaling in pancreatic acinar cells.

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“…Acute necrotizing pancreatitis complicating intestinal barrier functional disturbance (IBFD) is an important factor that leads to MODS. 23,24 When the intestinal barrier is damaged, DAO, which is secreted by intestinal cells, and D-lactate, which is produced by intestinal bacteria, transfer stage. Therefore, the detection of serum levels of DAO and D-lactate can be promptly reflected in the extent of damage and permeability changes in the small intestine, and they are the specificity and sensitivity indicators of intestinal barrier function evaluation.…”

Section: Discussionmentioning

confidence: 99%

Infliximab Enhances the Therapeutic Effectiveness of Octreotide on Acute Necrotizing Pancreatitis in Rat Model

Huang¹,

Li²,

Jia³

et al. 2012

Pancreas

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Pretreatment but not treatment with probiotics abolishes mouse intestinal barrier dysfunction in acute pancreatitis

Cited by 43 publications

References 38 publications

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Sensing of Commensal Organisms by the Intracellular Sensor NOD1 Mediates Experimental Pancreatitis

Infliximab Enhances the Therapeutic Effectiveness of Octreotide on Acute Necrotizing Pancreatitis in Rat Model

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