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PubMed2005

Aetiology of inflammatory bowel disease (IBD): role of intestinal microbiota and gut-associated lymphoid tissue immune response.

The aetiology of inflammatory bowel disease (IBD) probably involves a combination of genetic predisposition and environmental factors that may be channelled through an abnormality in gut-barrier function, with a loss of antigen tolerance. Some genetic markers that predispose to inflammatory disease have been identified (alleles DR2, DRB1*0103, DRB1*12 and mutations in the NOD2/CARD15 gene on chromosome 16). Alterations in the pattern of cytokine production by T cell subclasses leading to loss of tolerance to oral antigens have been documented. Moreover, a number of environmental factors (cigarette smoking, use of non-steroid anti-inflammatory drugs, psychological stress and the presence of the caecal appendix) have been postulated as a trigger of IBD. It has also been suggested that the gut microbiota plays a major role in the development and persistence of IBD, and numerous modifications of intestinal microbiota composition have been identified. As a result, manipulation of the microbiota with antibiotics is a current therapeutic strategy; more recently, however, a number of studies have reported promising results when using probiotic organisms to manipulate gut microbiota composition in order to restore tolerance to microbial antigens of the host's own microbiota.

Animals↗

PubMed2004

Inflammation rather than nutritional depletion determines glutamine concentrations and intestinal permeability.

AIM: Nutritional depletion has been correlated with low plasma and mucosal glutamine concentrations and with increased intestinal permeability. Since nutritional depletion often is associated with (chronic) inflammatory stress, this study was designed to establish the influence of depletion and inflammation on glutamine concentrations and gut barrier function. METHODS: Anthropometric parameters were calculated from 26 patients who required artificial nutrition. Glutamine concentrations in plasma and gut mucosa, gut permeability and mucosal morphology were assessed. For determination of the degree of inflammation erythrocyte sedimentation rates and (pre)albumin concentrations were measured. On the basis of these parameters patients were divided into two groups having significant inflammatory stress or not. Similarly, a depleted and a non-depleted group was formed based on percentage ideal body weight, fat-free mass index (FFMI) and percentage weight loss. Glutamine concentrations, gut permeability and villus morphology were compared between the groups. RESULTS: The presence of inflammatory activity had significant negative effects on glutamine concentrations in contrast to the presence or absence of nutritional depletion. Similarly, intestinal permeability increased during active inflammation but not in depleted patients. FFMI but not inflammation was related to villus height. CONCLUSIONS: The presence of inflammation significantly affects glutamine concentrations and gut permeability, in contrast to the presence of depletion of body cell mass per se. On the other hand, villus morphology is not influenced by changes in systemic inflammatory activity whereas nutritional status possibly does affect villus height.

Adult↗

PubMed2004

cDNA cloning and functional expression of a Ca2+-sensing receptor with truncated C-terminal tail from the Mozambique tilapia (Oreochromis mossambicus).

The complete cDNA sequence of the tilapia extracellular Ca(2+)-sensing receptor (CaR) was determined. The transcript length of tilapia CaR (tCaR) is 3.4 kbp and encodes a 940-amino acid, 7-transmembrane domain protein that is consistent in its structural features with known mammalian and piscine CaRs. The tCaR extracellular domain includes a characteristic hydrophobic segment, conserved cysteine residues that are implicated in receptor dimerization (Cys(129) and Cys(131)) and in coupling to the transmembrane domain (nine conserved cysteine residues), and conserved serine residues (Ser(147) and Ser(169-171)) that are linked to receptor binding of Ca(2+) and L-amino acid-mediated potentiation of function. mRNA expression of tCaR was strong in kidney, brain, and gill. Weaker expression was observed in pituitary, stomach, intestine, urinary bladder, and heart. This distribution is consistent with possible physiological roles in endocrine cells, excitable tissues, and ion-transporting barrier epithelia. Expression of tCaR mRNA in kidney and intestine was salinity-dependent, suggesting a role for the receptor in iono-/osmoregulation in this euryhaline teleost species. Human embryonic kidney-293 cells transiently transfected with tCaR cDNA demonstrated dose-dependent phospholipase C activation in response to elevations in the extracellular Ca(2+) concentration ([Ca(2+)](o)). Functional activation of the mitogen-activated protein kinase cascade by high [Ca(2+)](o) was also confirmed in these cells despite the naturally occurring truncation of the receptor's intracellular tail, which removes segments variably linked in mammalian CaRs to filamin-coupled activation of mitogen-activated protein kinase cascades. Sensitivity of phospholipase C activation to [Ca(2+)](o) was dependent on the ionic strength of the bathing medium, supporting a role in salinity sensing.

Amino Acid Sequence↗

PubMed2006

Regulation of the intestinal epithelial barrier by the apical junctional complex.

PURPOSE OF REVIEW: Epithelial intercellular junctions are important components of the epithelial barrier and are compromised in disorders such as Crohn's disease. We will highlight recent progress in understanding the role of an intercellular junction referred to as the apical junctional complex in regulating small intestinal epithelial permeability in health and disease. RECENT FINDINGS: Recent studies have implicated aberrant regulation of the AJC as an underlying factor contributing to a leaky epithelial barrier in Crohn's patients. Consequences of increased epithelial permeability include exposure of intestinal tissue to luminal antigens/pathogens which in turn influence disease activity. Furthermore, proinflammatory cytokines released into the milieu of the epithelium in patients with Crohn's disease influence apical junctional complex and epithelial barrier function. Such cytokines induce disassembly of the apical junctional complex by promoting differential endocytosis of component proteins. Additionally, apical junctional complex proteins are targeted by pathogens that use the epithelium as a portal of entry to establish disease in the host. SUMMARY: The epithelial apical junctional complex is important in determining epithelial barrier properties. Recent studies have highlighted contribution of proinflammatory cytokines and endocytosis of apical junctional complex proteins to the epithelial barrier defect. Continued advances in understanding of this field will yield new therapeutic targets for intestinal disorders.

Adherens Junctions↗

PubMed2006

Role of pharmacogenetics of ATP-binding cassette transporters in the pharmacokinetics of drugs.

Interindividual differences of drug response are an important cause of treatment failures and adverse drug reactions. The identification of polymorphisms explaining distinct phenotypes of drug metabolizing enzymes contributed in part to the understanding of individual variations of drug plasma levels. However, bioavailability also depends on a major extent from the expression and activity of drug transport across biomembranes. In particular efflux transporters of the ATP-binding cassette (ABC) family such as ABCB1 (P-glycoprotein, P-gp), the ABCC (multidrug resistance-related protein, MRP) family and ABCG2 (breast cancer resistance protein, BCRP) have been identified as major determinants of chemoresistance in tumor cells. They are expressed in the apical membranes of many barrier tissue such as the intestine, liver, blood-brain barrier, kidney, placenta, testis and in lymphocytes, thus contributing to plasma, liquor, but also intracellular drug disposition. Since expression and function exhibit a broad variability, it was hypothesized that hereditary variances in the genes of membrane transporters could explain at least in part interindividual differences of pharmacokinetics and clinical outcome of a variety of drugs. This review focuses on the functional significance of single nucleotide polymorphisms (SNP) of ABCB1, ABCC1, ABCC2, and ABCG2 in in vitro systems, in vivo tissues and drug disposition, as well as on the clinical outcome of major indications.

ATP-Binding Cassette Transporters↗

PubMedDate not supplied

[Digestive manifestations of food hypersensitivity in adults].

Food allergy, synonymous with food hypersensitivity (FHS), is defined as an immunologically-mediated adverse reaction to food. Initiation of FHS could result from a break in the immune mucosal barrier with abrogation of oral tolerance. Food hypersensitivity is mostly due to immediate-type reaction involving IgE-dependent mastocytes activation. Changes in intestinal function and structure have been mainly studies in an animal model of rat sensitized to egg albumin. Intraluminal antigen challenge resulted in abnormalities of gut absorption, secretion and motility in sensitized rats. In man, experimental data are scarce. Gastrointestinal manifestations of immediate FHS are varying and unspecific. A role for FHS in irritable bowel syndrome is debated. Participation of delayed-type FHS to digestive diseases is still questionable, but eosinophilic gastroenteritis might be an example. In clinical practice, diagnosis of FHS demands rigorous criteria. Double blind placebo-controlled food challenge has eventually proved to be the "gold standard" test for FHS diagnosis.

Animals↗

PubMed2004

Enteric glia.

The enteric nervous system is composed of both enteric neurones and enteric glia. Enteric glial cells were first described by Dogiel and are now known to outnumber neurones approximately 4 : 1. In the past, these cells were assumed to subserve a largely supportive role; however, recent evidence indicates that enteric glial cells may play a more active role in the control of gut function. In transgenic mouse models, where enteric glial cells are selectively ablated, the loss of glia results in intestinal inflammation and disruption of the epithelial barrier. Enteric glia are activated specifically by inflammatory insults and may contribute actively to inflammatory pathology via antigen presentation and cytokine synthesis. Enteric glia also express receptors for neurotransmitters and so may serve as intermediaries in enteric neurotransmission. Thus, enteric glia may serve as a link between the nervous and immune systems of the gut and may also have an important role in maintaining the integrity of the mucosal barrier and in other aspects of intestinal homeostasis.

Animals↗

PubMed2005

Anti-glycosyl antibodies in lipid rafts of the enterocyte brush border: a possible host defense against pathogens.

The pig small intestinal brush border is a glycoprotein- and glycolipid-rich membrane that functions as a digestive/absorptive surface for dietary nutrients as well as a permeability barrier for pathogens. The present work was performed to identify carbohydrate-binding (lectinlike) proteins associated with the brush border. Chromatography on lactose-agarose was used to isolate such proteins, and their localization was studied biochemically and by immunofluorescence microscopy and immunogold electron microscopy. IgG and IgM were the two major proteins isolated, indicating that naturally occurring anti-glycosyl antibodies are among the major lectinlike proteins in the gut. IgG and IgM as well as IgA were localized to the enterocyte brush border, and a brief lactose wash partially released all three immunoglobulins from the membrane, indicating that anti-glycosyl antibodies constitute a major part of the immunoglobulins at the lumenal surface of the gut. The antibodies were associated with lipid rafts at the brush border, and they frequently (52%) coclustered with the raft marker galectin 4. A lactose wash increased the susceptibility of the brush border toward lectin peanut agglutin and cholera toxin B, suggesting that anti-glycosyl antibodies compete with other carbohydrate-binding proteins at the lumenal surface of the gut. Thus anti-glycosyl antibodies constitute a major group of proteins associated with the enterocyte brush border membrane. We propose they function by protecting the lipid raft microdomains of the brush border against pathogens.

Animals↗

PubMed1987

Structure and function of intestinal mucin: developmental aspects.

Mucin glycoproteins are thought to play an important role in protecting the intestine from chemical or physical injury but the mechanisms of protection and the possible relationship between mucin structure and function are incompletely understood. Structurally, purified intestinal mucins are a heterogeneous and polydisperse group of large-molecular-weight glycoproteins which have regional and developmental differences in composition. Newborn mucin contains more protein and less carbohydrate than adult mucin and differs from adult mucin in buoyant density and mobility on electrophoresis. The primary function of mucin, protection of the intestine, appears to be dependent upon at least four factors: the rate and quantity of mucin release; the physical barrier of the viscous mucus blanket; the provision of specific inhibitory binding sites to infectious agents and proteins, and the inclusion of secretory immunoglobulins to provide a link to the immunologic component of the intestinal host defense system. Immune as well as infectious and chemical agents appear to play an important role in mucus release but developmental effects have not been studied. Preliminary studies indicate that developmental differences may exist in the provision of inhibitory binding sites and the inclusion of secretory immunoglobulins in mucin. These studies indicate that mucus may provide a link between the physical and immunological components of the intestinal host defense system and point to the need for further studies in this area.

Animals↗

PubMed2005

Cathepsin S controls MHC class II-mediated antigen presentation by epithelial cells in vivo.

Epithelial cells at environmental interfaces provide protection from potentially harmful agents, including pathogens. In addition to serving as a physical barrier and producing soluble mediators of immunity, such as cytokines or antimicrobial peptides, these cells are thought to function as nonprofessional APCs. In this regard, intestinal epithelial cells are particularly prominent because they express MHC class II molecules at the site of massive antigenic exposure. However, unlike bone marrow-derived professional APC, such as dendritic cells or B cells, little is known about the mechanisms of MHC class II presentation by the nonprofessional APC in vivo. The former use the lysosomal cysteine protease cathepsin S (Cat S), whereas thymic cortical epithelial cells use cathepsin L (Cat L) for invariant chain degradation and MHC class II maturation. Unexpectedly, we found that murine Cat S plays a critical role in invariant chain degradation in intestinal epithelial cells. Furthermore, we report that nonprofessional APC present a class II-bound endogenous peptide to naive CD4 T cells in vivo in a Cat S-dependent fashion. These results suggest that in vivo, both professional and nonprofessional MHC class II-expressing APC use Cat S, but not Cat L, for MHC class II-mediated Ag presentation.

Animals↗

PubMed1999

[Practical aspects of early enteral feeding].

"Gut injury" and a corresponding impaired gut barrier function are thought to have a high impact on the development of multiple organ failure (MOF) in the critically ill. Mucosal lesions and increased intestinal permeability can provoke translocation of bacteria and endotoxins and initiate local and/or systemic immune-inflammatory response, bearing the risk of development of multiple organ failure. Enteral nutrition using the physiological pathway provides the intestinal mucosa with nutrients, which is thought to reduce bacterial translocation and septic complications. Considerable gastric reflux and delayed bowel motility are the principal problems of enteral nutrition. Therefore, in the early postoperative period at least a nasoduodenal or--jejunal feeding tube or feeding jejunostomy is required. The commonly used enteral formulas are well tolerated. So-called "immunonutrition" includes special formulas supplemented with immunemodulating substances like arginine, omega-3-fatty acids, ribonucleic acids and glutamine. Some beneficial effects of immune-enhancing diets have recently been reported for immune response, infectious complication rate, systemic inflammatory response syndrome (SIRS), multiple organ failure (MOF), antibiotic usage and length of hospital stay, especially in patients after trauma or surgery. However, the definite role is still unknown and indications have still to be defined. Enteral feeding should start with small volumes, the amount being gradually increased according to a patient's individual tolerance. Common problems are gastric reflux, diarrhoea and distension, but usage of a suitable formula, a gradual increase or reduction in the amount of enteral feeding and, additionally, parenteral nutrition can help to overcome such complications. Clinical examination of the enterally fed patient should be performed carefully. Standard nutritional monitoring of electrolytes, glucose, triglycerides, cholinesterase, albumin, differential blood count, urine-glucose and nitrogen retention to assess the catabolic state should be performed routinely. Although only little data from randomised trials are available, enteral nutrition has advantages and is cheaper than total parenteral nutrition. In the critically ill, the goal of enteral feeding is not coverage of total caloric requirements, but continuous administration of at least a small amount in order to prevent gut mucosa atrophy. Nutrition is an important aspect in critical care medicine, and enteral feeding should be attempted at least partially.

Critical Care↗

PubMed1990

[Damage in the hemato-enteral barrier in experimental liver transplantation].

Semiquantitative analyzes of intestinal mucous lesion graduating from 0 (normal) to V (necrotic) were done in the experimental model, 6-12h alter the heterotopic liver transplantation in dogs. All degrees of mucous damages were found in intestinal samples (mean value was 2.60). The most dominant were the lesions of III (31%) and IV (25%) degree while in 4% complete destruction of mucousal villious was observed. Success of liver transplantation besides the presence of the lesions of hepatic alograft during the phases of the warm and cold ischemia or immunological responses, depends on the changes in functionally connected regions. In that sense the damages of mesenterial department lead a very important role. Lumenal infective agents and cardiodepressive macromolecules, passing trough the hematoenteral barrier, cause local hepatic damages and central cardiovascular failure.

Animals↗

PubMed1998

The effect of epidermal growth factor on bacterial translocation in newborn rabbits.

PURPOSE: Epidermal growth factor (EGF), which is present in breast milk, has both trophic and maturational effects on intestinal mucosa. The aim of this study is to determine the effect of EGF on spontaneous intestinal bacterial translocation (BT) in formula-fed newborn rabbits, who have a high incidence of BT compared with breast-fed newborn rabbits. METHODS: Sixty-one rabbit pups were divided into three groups: EGF(-), n=24, EGF(+), n=22, and breast-fed animals, n=15. Both the EGF(-) and EGF(+) groups were gavage fed a standard artificial formula three times daily. EGF was administered subcutaneously three times daily (1.5 microg/g body weight per day) in the EGF(+) group. The breast-fed group was fed by their mothers ad libitum. At 7 days of age, all rabbits were killed, and the mesenteric lymph nodes (MLN), liver, and spleen were cultured qualitatively for bacterial growth, while the cecum and ileum were quantitatively cultured. To determine the effect of EGF on mucus-producing cells, goblet cell numbers in the small intestine were quantified histologically. RESULTS: There was no BT to MLN, spleen, or liver in the breast-fed group. The incidence of BT to MLN and spleen was significantly lower in the EGF(+) compared with EGF(-) group; (EGF[+]: MLN, 45%; spleen, 32%; Liver, 27%; EGF[-]: MLN, 79%; Spleen 67%; Liver 29%; in EGF[+] MLN and Spleen P<.05 vEGF[-]). There was no significant difference in cecal and ileal bacterial colonization between the EGF(+) and EGF(-) groups. The number of goblet cells in the small intestine was significantly lower in the EGF(-) group compared with the EGF(+) group as follows: EGF(+), 14+/-3; EGF(-), 9+/-3; breast-fed, 11+/-5 goblet cells per 100 epithelial cell nuclei; P=.013. CONCLUSIONS: (1) EGF caused a significant decrease in spontaneous bacterial translocation in formula-fed newborn rabbits and was associated with an increase in the goblet cell number of the small intestine. (2) These changes occurred in spite of the fact that no changes in small bowel bacterial colonization were observed. (3) These results suggest, but do not prove, that EGF may provide protection for neonates from gut origin infection by improving the mucosal barrier function through increased goblet cell production, thus decreasing the incidence of spontaneous bacterial translocation in the newborn.

Animals↗

PubMed1998

Immunoglobulin A supplementation abrogates bacterial translocation and preserves the architecture of the intestinal epithelium.

BACKGROUND: Breast milk has been shown to prevent gut-origin infections in neonates through undefined mechanisms. Putative protective factors in breast milk include immunoglobulin (Ig)A, IgG, and lactoferrin. We examined their role in bacterial translocation in neonatal rabbits. METHODS: IgA, IgG, and lactoferrin were isolated from rabbit breast milk through gel filtration and ion-exchange chromatography. Neonates were randomized to receive breast milk, formula alone, or formula supplemented with IgA, IgG, or lactoferrin. Quantitative cultures were performed on day 7 for bacterial translocation. Hematoxylin-eosin-stained sections of distal ileum were examined by light microscopy. Transmucosal bacterial passage was determined in vitro, and the ileal mucosal membranes were examined by confocal microscopy. RESULTS: IgA supplementation abrogated bacterial translocation. IgG and lactoferrin had no significant effect. Neonates that received IgA or breast milk gained more weight than those in the other groups. IgA reduced transmucosal bacterial passage in vitro. In contrast to the normal-appearing distal ileum of neonates fed breast milk, intestinal epithelium from neonates that received formula or formula with IgG or IgA demonstrated prominent vacuoles by light microscopy. Those fed formula alone or formula with lactoferrin had slightly shortened villi. CONCLUSIONS: IgA supplementation prevents bacterial translocation by enhancing gut mucosal barrier function.

Animals↗

PubMed2003

Simultaneous onset of acute inflammatory response, sepsis-like symptoms and intestinal mucosal injury after cancer chemotherapy.

Chemotherapy is 1 method for the treatment of cancer, but serious side effects can sometimes limit the dosage given. Mild fever and diarrhea are common side effects of cancer chemotherapy. Gastrointestinal injury induced by chemotherapeutic agents may result in bacterial/endotoxin translocation from the gut into the systemic circulation. An experimental study was therefore conducted to clarify the effect of systemic chemotherapeutic agents on gastrointestinal barrier function. Male Wistar rats were divided into a 5-fluorouracil (5-FU) group (100 mg/kg/day for 4 days; n = 27) and a control group (n = 5). All rats were fasted and central venous catheterization was performed for total parenteral nutrition and blood sampling. Intestinal tissue was also sampled for pathological examination. Plasma levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) were determined by ELISA, bacterial translocation was quantified by lymph node culture and plasma endotoxin content of portal blood was measured by the Limulus-amebocyte-lysate test. In the 5-FU group on day 4, a proportion of rats exhibited severe watery diarrhea (73.9%) and occasional vomiting (86.2%). The levels of plasma TNFalpha and IL-6 were seen to increase, peaking at day 6 (IL-6, 350.0 +/- 67.8 pg/ml; TNFalpha, 26.1 +/- 3.2 pg/ml). The pathological findings also changed on day 4. On day 6, 90% of the rats in the 5-FU group showed dramatic sepsis-like manifestations, whereas the control group did not. Within the 5-FU group, only at day 6 was bacterial translocation in the rat mesenteric lymph nodes or significantly elevated levels of endotoxin evident. These results suggest that bacterial/endotoxin translocation might cause sepsis-like manifestations after systemic chemotherapy.

Animals↗

PubMed2002

Intestinal absorption enhancement of the ester prodrug tenofovir disoproxil fumarate through modulation of the biochemical barrier by defined ester mixtures.

The effect of discrete esters and ester mixtures on the intestinal stability and absorption of tenofovir disoproxil fumarate (tenofovir DF, an esterase-sensitive prodrug of the antiviral tenofovir) was compared with the effect of strawberry extract, which has been shown to enhance the absorption of the prodrug across Caco-2 monolayers and in rat ileum. In addition, the mechanism of absorption enhancement was investigated. In rat intestinal homogenates, complete inhibition of the conversion of tenofovir DF (as obtained by strawberry extract) could only be obtained at relatively high concentrations of the discrete esters or by using mixtures of esters (e.g., propyl p-hydroxybenzoate 0.02%, octyl acetate 0.02%, ethyl caprylate 0.01%). Coincubation of tenofovir DF with this mixture also resulted in an enhancement of its absorption in the in vitro Caco-2 system as well as in rat ileum. As tenofovir DF is a substrate for P-glycoprotein (P-gp)-related efflux carriers in the Caco-2 model, the modulatory effect of the ester mixtures was studied on the functionality of P-gp using cyclosporin A (CsA) as a model substrate. Strawberry extract as well as the mixture of three esters interfered with the absorptive transport of CsA across Caco-2 monolayers, illustrating that both mixtures interfere with both esterase-activity and P-gp functionality. This concerted barrier was not observed in rat ileum, suggesting differential functional activities of the biochemical barrier toward tenofovir DF in different absorption systems. Overall, our results illustrate that modulation of the biochemical barrier (metabolism and efflux) of tenofovir DF by ester mixtures can be used to increase the intestinal absorption of tenofovir DF in an in vitro and an in situ absorption model; the mechanism of action appears to be a complex interplay of different systems; the differential expression of carriers and enzymes in different systems illustrates the difficulty of extrapolating observations between different systems/species.

Adenine↗

PubMed2002

The functions of mucosal T cells in containing the indigenous commensal flora of the intestine.

There is an immense load of non-pathogenic commensal bacteria in the distal small intestine and the colon of mammals. The physical barrier that prevents penetration (translocation) of these organisms into the body is a simple epithelium comprised of the single enterocyte/colonocyte cell layer with its overlying mucus. In this review, we discuss the roles of intestinal T cells in initiating and regulating innate and adaptive mucosal immune responses of the mucosal immune system that avoid or limit penetration of the commensal intestinal bacteria.

Animals↗

PubMed2004

Intestinal epithelial cell regulation of mucosal inflammation.

The intestinal epithelium serves as one of human's primary interfaces with the outside world. This interface is very heavily colonized with bacteria and yet permits absorption of life-sustaining nutrients while protecting the tissues below from microbial onslaught. Although the gut epithelium had been classically thought to achieve this function primarily by functioning as a passive, albeit highly selective, barrier, research over the last decade has demonstrated that in fact the epithelium plays a very active role in protecting the host from the bacteria that colonize it. As a consequence of its mediation of mucosal immunity, intestinal epithelial dysfunction appears to be central to diseases associated with aberrant gut mucosal immune responses such as inflammatory bowel disease (IBD). This article reviews: (1) how the gut epithelium participates in regulating innate immune inflammatory responses to enteric pathogens, (2) how these responses may regulate the adaptive immune system, (3) mechanisms that may resolve acute inflammation, and (4) how epithelial dysfunction may participate in regulating both the active and chronic phases of IBD.

Bacteria↗