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Association Between Exercise-Induced Hyperthermia and Intestinal Permeability: A Systematic Review.
Pires, W, Veneroso, CE, Wanner, SP, Pacheco, DAS, Vaz, GC, Amorim, FT, Tonoli, C, Soares, DD, Coimbra, CC
Sports medicine (Auckland, N.Z.). 2017;(7):1389-1403
Abstract
BACKGROUND Prolonged and strenuous physical exercise increases intestinal permeability, allowing luminal endotoxins to translocate through the intestinal barrier and reach the bloodstream. When recognized by the immune system, these endotoxins trigger a systemic inflammatory response that may affect physical performance and, in severe cases, induce heat stroke. However, it remains to be elucidated whether there is a relationship between the magnitude of exercise-induced hyperthermia and changes in intestinal permeability. OBJECTIVE In this systematic review, we evaluated whether an exercise-induced increase in core body temperature (T Core) is associated with an exercise-induced increase in intestinal permeability. METHODS The present systematic review screened the MEDLINE/PubMed and Web of Science databases in September 2016, without any date restrictions. Sixteen studies that were performed in healthy participants, presented original data, and measured both the exercise-induced changes in T Core and intestinal permeability were selected. These studies assessed intestinal permeability through the measurement of sugar levels in the urine and measurement of intestinal fatty acid binding protein or lipopolysaccharide levels in the blood. RESULTS Exercise increased both T Core and intestinal permeability in most of the 16 studies. In addition, a positive and strong correlation was observed between the two parameters (r = 0.793; p < 0.001), and a T Core exceeding 39 °C was always associated with augmented permeability. CONCLUSION The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.
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2.
[Future therapeutics in celiac disease].
Lerner, A
Harefuah. 2012;(6):358-61, 377
Abstract
Celiac disease is a common autoimmune disease affecting 1% of the Western populations. It is an inappropriate immune response, in genetically susceptible patients to dietary wheat, rye, barley and oats. Treatment involves a Lifelong gluten-free diet that predisposes to low compliance due to limited variety, high cost and low palatability, imposing social pressure and affecting quality of life. The result is an urgent need for alternative therapeutic strategies. Based on the growing actual knowledge on the intestinal inflammatory cascade, mucosal immunology and genetics of celiac disease, new attractive potential therapies are emerging. Possibilities include: searching for low immunogenic wheat variants or strains pretreated with enzymes or binders for lower toxicity. Other strategies involve decreasing transepithelial uptake or dampening of the adaptive immune response by transglutaminase inhibitors or blockage of the HLA groove and immune modulation to shift the TH1 to TH2 profile. Developing biological therapy aims to decrease intestinal homing, adhesion and activity of inflammatory cells, counteract the pro-inflammatory cytokines, clonal intestinal T cells or mesenchymal stem cell replacement or mitogenic intestinal repair safety, cost, affordability and clinical effectiveness are of prime concern. Most of the above strategies showed promising results ex-vivo. The future will highlight the in-vivo winner.
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3.
Influence of inflammatory disorders and infection on iron absorption and efficacy of iron-fortified foods.
Hurrell, RF
Nestle Nutrition Institute workshop series. 2012;:107-16
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Abstract
The provision of iron- fortified foods is a common strategy to prevent iron deficiency; however, ensuring adequate iron absorption is a challenge. Iron bioavailability depends on the choice of iron compound, the presence enhancers and inhibitors of absorption in the food matrix, and the physiological state of the consumer, including iron status, other nutritional deficiencies and inflammatory disorders. Inflammation associated with infections and inflammatory disorders would be expected to decrease iron absorption and reduce the efficacy of iron- fortified foods. The decreased absorption is due to an increase in circulating hepcidin in response to inflammatory cytokines. Hepcidin degrades ferroportin and blocks the passage of iron from the intestinal cell to the plasma. This is the innate immune response to infections and aims to restrict pathogen growth by restricting iron supply. Stable isotope studies have reported women and children with chronic malaria parasitemia or febrile malaria to have increased inflammatory cytokines, increased hepcidin and much decreased iron absorption. No studies have specifically investigated the efficacy of iron- fortified foods in the absence and presence of infections. In contrast, inflammation and increased hepcidin associated with adiposity in overweight have been linked to both lower iron absorption and the decreased efficacy of iron- fortified foods.
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Importance of disrupted intestinal barrier in inflammatory bowel diseases.
Salim, SY, Söderholm, JD
Inflammatory bowel diseases. 2011;(1):362-81
Abstract
The current paradigm of inflammatory bowel diseases (IBD), both Crohn's disease (CD) and ulcerative colitis (UC), involves the interaction between environmental factors in the intestinal lumen and inappropriate host immune responses in genetically predisposed individuals. The intestinal mucosal barrier has evolved to maintain a delicate balance between absorbing essential nutrients while preventing the entry and responding to harmful contents. In IBD, disruptions of essential elements of the intestinal barrier lead to permeability defects. These barrier defects exacerbate the underlying immune system, subsequently resulting in tissue damage. The epithelial phenotype in active IBD is very similar in CD and UC. It is characterized by increased secretion of chloride and water, leading to diarrhea, increased permeability via both the transcellular and paracellular routes, and increased apoptosis of epithelial cells. The main cytokine that seems to drive these changes is tumor necrosis factor alpha in CD, whereas interleukin (IL)-13 may be more important in UC. Therapeutic restoration of the mucosal barrier would provide protection and prevent antigenic overload due to intestinal "leakiness." Here we give an overview of the key players of the intestinal mucosal barrier and review the current literature from studies in humans and human systems on mechanisms underlying mucosal barrier dysfunction in IBD.
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Function of the intestinal epithelium and its dysregulation in inflammatory bowel disease.
Henderson, P, van Limbergen, JE, Schwarze, J, Wilson, DC
Inflammatory bowel diseases. 2011;(1):382-95
Abstract
The intestinal epithelium not only acts as a physical barrier to commensal bacteria and foreign antigens but is also actively involved in antigen processing and immune cell regulation. The inflammatory bowel diseases (IBDs) are characterized by inflammation at this mucosal surface with well-recognized defects in barrier and secretory function. In addition to this, defects in intraepithelial lymphocytes, chemokine receptors, and pattern recognition receptors promote an abnormal immune response, with increased differentiation of proinflammatory cells and a dysregulated relationship with professional antigen-presenting cells. This review focuses on recent developments in the structure of the epithelium, including a detailed account of the apical junctional complex in addition to the role of the enterocyte in antigen recognition, uptake, processing, and presentation. Recently described cytokines such as interleukin-22 and interleukin-31 are highlighted as is the dysregulation of chemokines and secretory IgA in IBD. Finally, the effect of the intestinal epithelial cell on T effector cell proliferation and differentiation are examined in the context of IBD with particular focus on T regulatory cells and the two-way interaction between the intestinal epithelial cell and certain immune cell populations.
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Efficacy of budesonide therapy in the early phase of treatment of adult coeliac disease patients with malabsorption: an in vivo/in vitro pilot study.
Ciacci, C, Maiuri, L, Russo, I, Tortora, R, Bucci, C, Cappello, C, Santonicola, A, Luciani, A, Passananti, V, Iovino, P
Clinical and experimental pharmacology & physiology. 2009;(12):1170-6
Abstract
1. Budesonide is a glucocorticosteroid with a local anti-inflammatory effect. Coeliac disease is an immune-mediated disease caused by gluten ingestion in intolerant patients. The aim of the present study was to investigate the efficacy of budesonide in malabsorptive coeliac patients and its effect in an in vitro gliadin challenge. 2. Twenty coeliac patients with malabsorption were enrolled in the present study and were randomly assigned to one of two 4 week treatments: (i) a gluten-free diet alone; or (ii) a gluten-free diet plus 6 mg budesonide daily. At the end of 4 weeks treatment, all patients underwent clinical evaluation, laboratory tests and self-evaluation of well-being using a visual analogue scale. Intestinal biopsies from five coeliac patients (selected randomly) and four non-coeliac disease controls who underwent upper endoscopy for intestinal bleeding were challenged with gliadin (0.5 mg/mL) and budesonide (10-30 microg/mL) for 3 and 24 h. Biopsies were tested by immunohistochemistry and immunofluorescence for known markers of inflammation. 3. Treatment of patients with 6 mg budesonide daily for 4 weeks resulted in increased bodyweight, a decreased number of evacuations and decreased stool weight compared with patients on a gluten-free diet alone for 4 weeks. Well-being scores were higher in patients treated with both a gluten-free diet and budesonide compared with those receiving a gluten-free diet alone. 4. In vitro studies showed that budesonide reduced epithelial tyrosine phosphorylation and expression of histocompatibility leucocyte antigen complex DR (HLA-DR) elicited by gliadin-derived peptides. In addition, the expression of cyclo-oxygenase (COX)-2 and intercellular adhesion molecule (ICAM)-1 in the lamina propria was reduced in patients treated with both gliadin and budesonide compared with patients treated with gliadin alone. Budesonide alone decreased HLA-DR in crypt enterocytes, as well as ICAM-1 and COX-2 expression in the lamina propria of biopsy specimen of coeliac patients. Budesonide had no effect in control samples. 5. In conclusion, the results of the present study indicate that budesonide shows efficacy in the treatment of symptoms in adult coeliac patients with overt malabsorption. The mechanism underlying the effects of budesonide in reducing symptoms was elucidated by in vitro studies involving a gliadin challenge.
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Prebiotic ingestion does not improve gastrointestinal barrier function in burn patients.
Olguin, F, Araya, M, Hirsch, S, Brunser, O, Ayala, V, Rivera, R, Gotteland, M
Burns : journal of the International Society for Burn Injuries. 2005;(4):482-8
Abstract
Prebiotics increase intestinal levels of health-promoting bacteria implicated in decreasing pathogen colonization, stimulating immune functions and stabilizing gut barrier functions, parameters which are altered in burn patients. We propose that regular intake of a prebiotic, oligofructose (OF), might help to improve the altered gastrointestinal (GI) permeability observed in burn patients. A randomized, double-blind, controlled clinical trial was carried out in 41 burn patients (mean burn surface area=17.1+/-8.2%) who ingested daily 6 g of oligofructose (OF group) or sucrose as placebo (Control group) during 15 days. Gastrointestinal permeability to sucrose and lactulose/mannitol (L/M) was evaluated on days 1 (before treatment) 3, 7, 14 and 21. A permeability test was also performed in 18 healthy subjects as controls. Thirty-one patients completed the protocol (dropout rate=24.4%). Healthy subjects had a basal sucrose excretion of 21.3 mg (14.0-32.5 mg) and a basal L/M ratio of 0.017% (0.009-0.022%). Sucrose excretion increased 5-fold and L/M ratio 4.4-fold in burn patients on day 1 and these high levels of marker excretion decreased significantly throughout the study (p=0.016 and 0.000001, respectively). No differences between the OF and Control groups were observed for sucrose excretion or L/M ratio. In conclusion, the normalization of gastrointestinal permeability is not accelerated by prebiotic intake.
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Gut barrier dysfunction in food allergy.
Heyman, M
European journal of gastroenterology & hepatology. 2005;(12):1279-85
Abstract
Intestinal permeability tests used in the diagnosis of allergic diseases in response to oral food challenge have led to the conclusion that constitutive defects of the intestinal barrier are not the primary cause of allergic diseases. However, perturbation of environmental factors (infection, stress), by increasing intestinal permeability and enhancing danger signals, may favour food allergy in susceptible individuals. The mechanisms of enhanced permeability to specific and bystander antigens have been delineated as well as the molecular events involved in the sequential phases of allergic reactions. Intestinal absorption of food antigens and immune responses are mutually dependent, and luminal (environmental) and serosal (intrinsic) factors synergize to maintain a self-perpetuating cycle in which antigens penetrate the mucosa and induce allergic inflammation.
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Feeding mode, intestinal permeability, and neopterin excretion: a longitudinal study in infants of HIV-infected South African women.
Rollins, NC, Filteau, SM, Coutsoudis, A, Tomkins, AM
Journal of acquired immune deficiency syndromes (1999). 2001;(2):132-9
Abstract
Exclusive breast feeding has been associated with a lower rate of mother-to-child HIV transmission than breast feeding plus other foods. To obtain further information on biologic outcomes of different feeding modes, we examined 272 infants of HIV-infected South African women at ages 1, 6, and 14 weeks. At each visit information about infant diet and morbidity was collected and infants underwent a lactulose/mannitol dual sugar intestinal permeability test. In a subset of infants, urinary neopterin excretion was measured as an indicator of immune system activation. Infants who had themselves become HIV-infected by 14 weeks had higher ( p <.01) intestinal permeability at 6 and 14 weeks and slightly (.05 < p <.1) higher neopterin excretion at all times than uninfected infants. At 1 week infants given no breast milk had higher ( p <.05) intestinal permeability than infants given breast milk exclusively or with other foods. Intestinal permeability in infants fed breast milk plus other foods was never increased relative to that of exclusively breastfed infants. Feeding mode had no effect on neopterin excretion. Thus, infant HIV infection induces changes in gut permeability and possibly immune system activation before clinical symptoms become apparent. The effects of feeding mode on infant intestinal permeability or urinary neopterin excretion do not explain a possible protective effect of exclusive breast feeding on mother-to-child transmission of HIV.
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10.
Barrier dysfunction and Crohn's disease.
Meddings, J
Annals of the New York Academy of Sciences. 2000;:333-8
Abstract
Crohn's disease is a debilitating illness of unknown etiology. A current hypothesis of disease pathogenesis suggests that this illness represents an abnormal immunological reaction to a luminal antigen. As part of this theory it is suggested that the luminal antigen is delivered to the mucosal immune system by a paracellular route. If this theory is correct several testable predictions can be made. In this manuscript these predictions are presented and the evidence to support or refute them is presented.