Tight junctions, leaky intestines, and pediatric diseases. Acta Paediatr
University of Florida, Gainesville, Florida, United States Acta Paediatrica
(Impact Factor: 1.67).
05/2005; 94(4):386-93. DOI: 10.1111/j.1651-2227.2005.tb01904.x
Tight junctions (TJs) represent the major barrier within the paracellular pathway between intestinal epithelial cells. Disruption of TJs leads to intestinal hyperpermeability (the so-called "leaky gut") and is implicated in the pathogenesis of several acute and chronic pediatric disease entities that are likely to have their origin during infancy.
This review provides an overview of evidence for the role of TJ breakdown in diseases such as systemic inflammatory response syndrome (SIRS), inflammatory bowel disease, type 1 diabetes, allergies, asthma, and autism.
A better basic understanding of this structure might lead to prevention or treatment of these diseases using nutritional or other means.
Available from: PubMed Central
- "The tight junction (TJ) proteins expressed in the cells play a key role in intestinal barrier function by protecting against toxic substances, allergens, and macromolecules derived from food . However, dysfunction or destruction of TJ may cause inflammatory diseases such as inflammatory bowel disease, irritable bowel syndrome , leaky gut syndrome, and food allergy    . Recently, various components derived from food and plants have been known to enhance intestinal barrier function. "
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ABSTRACT: Fructus Arctii is used as a traditional herbal medicine to treat inflammatory diseases in oriental countries. This study aimed to investigate effect of F. Arctii extract on intestinal barrier function in human intestinal epithelial Caco-2 cells and to reveal the active component of F. Arctii. We measured transepithelial electrical resistance (TEER) value (as an index of barrier function) and ovalbumin (OVA) permeation (as an index of permeability) to observe the changes of intestinal barrier function. The treatment of F. Arctii increased TEER value and decreased OVA influx on Caco-2 cell monolayers. Furthermore, we found that arctigenin as an active component of F. Arctii increased TEER value and reduced permeability of OVA from apical to the basolateral side but not arctiin. In the present study, we revealed that F. Arctii could enhance intestinal barrier function, and its active component was an arctigenin on the functionality. We expect that the arctigenin from F. Arctii could contribute to prevention of inflammatory, allergic, and infectious diseases by reinforcing intestinal barrier function.
Available from: Stefanie Niederlechner
- "Defects in intestinal epithelial barrier function have been proposed to play a role in a range of diseases such as the systemic inflammatory response syndrome (SIRS), sepsis, inflammatory bowel disease, asthma, allergies, type 1 diabetes, cardiovascular disease, and even autism     . Intestinal health-targeted therapeutic agents able to preserve intestinal barrier function have significant clinical implications in both prevention and treatment of these disease states. "
Available from: Myron Sasser
- "''Leaky gut'' syndrome ''Leaky Gut'' Syndrome is a term given to the condition where the epithelial barrier function of the small or large intestine is impaired , causing less discrimination in the numbers and types of molecules and cells that are able to pass from the gut to the circulatory system and vice versa   . Tight junctions are responsible for the epithelial barrier function, and consist of a system of several proteins in the paracellular space between each cell in the gut lining. "
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ABSTRACT: Autism Spectrum Disorders are neurodevelopmental disorders with symptoms that include cognitive impairments, stereotyped behaviors, and impairments in social skills. The dramatic increase in incidence of autism in recent years has created an increased need to find effective treatments. This paper proposes a hypothesis for a systems model of the connections between Autism Spectrum Disorder pathogenesis routes observed in recent studies. A combination treatment option is proposed to combat multiple pathogenesis mechanisms at once. Autism has been cited as being linked to gastrointestinal symptoms and is thought to be caused by a combination of genetic predisposition and environmental factors. Neuroinflammation as a result of increased gastrointestinal permeability has been noted as being a likely cause of Autism Spectrum Disorders, with possible primary causes stemming from abnormal intestinal bacteria and/or sulfur metabolic deficiencies. Our pathogenesis model proposes a circular relationship: oxidative stress and sulfur metabolic deficiencies could cause changes in colonic bacterial composition; and environmental bacterial contaminants could lead to elevated oxidative stress in individuals. It would thus be a self-perpetuating process where treatment options with single targets would have short-lived effects. It is believed that bacterial toxins, oxidative stress and dietary allergens such as gluten could all lead to increased epithelial permeability. Therefore, we propose a combination treatment to combat intestinal permeability, abnormal bacteria and/or bacterial overgrowth, and sulfur metabolic deficiencies. It is our hope that the proposed model will inspire new studies in finding effective treatments for individuals with Autism Spectrum Disorders. We suggest possible future studies that may lend more credibility to the proposed model.
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