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PubMed2002

The prostaglandin receptor EP4 suppresses colitis, mucosal damage and CD4 cell activation in the gut.

We used mice deficient in each of the eight types and subtypes of prostanoid receptors and examined the roles of prostanoids in dextran sodium sulfate-induced (DSS-induced) colitis. Among the prostanoid receptor-deficient mice, only EP4-deficient mice and not mice deficient in either DP, EP1, EP2, EP3, FP, IP, or TP developed severe colitis with 3% DSS treatment, which induced only marginal colitis in wild-type mice. This phenotype was mimicked in wild-type mice by administration of an EP4-selective antagonist (AE3-208). The EP4 deficiency impaired mucosal barrier function and induced epithelial loss, crypt damage, and aggregation of neutrophils and lymphocytes in the colon. Conversely, administration of an EP4-selective agonist (AE1-734) to wild-type mice ameliorated severe colitis normally induced with 7% DSS, while that of AE3-208 suppressed recovery from colitis and induced significant proliferation of CD4+ T cells. In vitro AE3-208 enhanced and AE1-734 suppressed the proliferation and Th1 cytokine production of lamina propria mononuclear cells from the colon. DNA microarray analysis revealed elevated expression of genes associated with immune response and reduced expression of genes with mucosal repair and remodeling in the colon of EP4-deficient mice. We conclude that EP4 maintains intestinal homeostasis by keeping mucosal integrity and downregulating immune response.

Animals↗

PubMed2001

Flavonoid antioxidants.

In order to ascertain the role of dietary flavonoids as antioxidants in vivo it is necessary to understand the chemical nature of the absorbed forms in the circulation in vivo and how the multiplicity of research findings in vitro reflect the bioactivity of flavonoids in vivo. Only when we gain adequate information on the circulating forms can we begin to understand the targeting to the tissues, whether flavonoids cross the blood-brain barrier, for example, and in what forms. Flavonoids are powerful antioxidants in vitro, but their overall function in vivo has yet to be clarified, whether antioxidant, anti-inflammatory, enzyme inhibitor, enzyme inducer, inhibitor of cell division, or some other role. It should also be emphasised that the reducing properties of flavonoids might contribute to redox regulation in cells, independently of their antioxidant properties, and thus might protect against cell ageing, for example, by working together with the intracellular reductant network. To gain understanding of these issues the factors influencing the absorption of flavonoids in the gastrointestinal tract needs to be established, namely the questions of: de-glycosylation before absorption, conjugation in the small intestine through glucuronidation, sulphation or methylation etc, metabolism and degradation in the colon to smaller phenolic molecules. The forms in which they circulate in vivo will influence their polarity and, thus, their localization and bioactivities in vivo. Finally if antioxidant activities are important, the elucidation of how such properties in vitro relate to the potential for conjugates and metabolites in vivo to act as antioxidants is required. The absorbed flavonoid components might function in the aqueous phase (like vitamin C) or in the lipophilic milieu (as vitamin E) in vivo. This will depend on their polarity properties on uptake, how they are metabolised on absorption, and their resulting structural forms in the circulation.

Antioxidants↗

PubMed1980

Intestinal electrophysiology and transmural ion transport in freshwater prawns.

A steady-state transmural potential difference of 1.63 +/- 0.26 mV (mean +/- SE, lumen negative) is recorded across the isolated, perfused intestine of the freshwater prawn, Macrobrachium rosenbergii, when saline approximating hemolymph in composition is present on both surfaces of the preparation. The magnitude of this potential is a hyperbolic function of bilateral K concentration. It is abolished by metabolic poinsons (NaN3 and iodoacetate) or ouabain and appears to result largely from the combined net transmural fluxes of Na, Cl, and K. Net fluxes of Na (1,49 +/- 0;30 mu mol . cm-2 . h-1) and Cl (0.72 +/- 0.22) are absorptive, whereas that of K (0.47 +/- 0.11) IS SECRETORY. Bilateral absence of Na abolishes net K secretion, whereas bilateral addition of ouabain (0.5 mM) eliminates net Na absorption. One-third of net K secretion appears to be transcellular and coupled to the net cellular transfer of Na in the opposite direction. The remaining component of K secretion can be attributed to paracellular cation flow responsive to transmural PD, Transmural diffusion potentials generated in the presence and absence of metabolic poisons provide the following passive permeability properties of the tissue: PK:PNa:PCl = 5.1:1.1:0.5. The symmetrical nature of these diffusion potentials implies the occurrence of a single rate-limiting barrier to ion flow with the above characteristics--probably the cell junction (septate desmosome) and paracellular channel. A model for transepithelial ion transport is presented where transmural potential difference is largely a result of an apparent 9 Na/1 K basolateral cationic exchange.

Animals↗

PubMed1993

Oral prostaglandin E2 prevents gut atrophy during intravenous feeding but not bacterial translocation.

The pathophysiologic changes in gut physiology that result in bacterial translocation during intravenous feeding are poorly defined, though believed to be related in part to intestinal atrophy, decreased mesenteric blood flow, and lack of intestinal secretions. This study investigated the hypothesis that pharmacologic preservation of intestinal structure and function by orally administered 16,16-dimethyl-prostaglandin E2 would prevent bacterial translocation in intravenously fed rats. Thirty-five rats were randomized to three groups: group 1 was fed rat chow ad libitum, group 2 received standard parenteral nutrition, and group 3 received parenteral nutrition plus oral 16,16-dimethyl-prostaglandin E2 (150 micrograms/kg twice a day). Rats were fed there respective diets for 5 days and killed. Mesenteric lymph nodes were procured for culture, and the intestine was assessed for weight, DNA, protein values, and histologic character. Results demonstrate that orally administered 16,16-dimethyl-prostaglandin E2 potently attenuates the intestinal atrophy associated with parenteral feeding but does not prevent bacterial translocation. Intestinal barrier dysfunction and bacterial translocation during intravenous feeding is related to factors other than the development of gut atrophy.

Administration, Oral↗

PubMed1993

Using enteral nutrition formulas.

A review of enteral tube feeding formulations is presented. When choosing an enteral formula product for a patient one must first determine the calorie and protein needs of the patient. Then one must determine the level of gastrointestinal tract function. First ask, to what degree is the small bowel functioning: totally, partially, or not at all? Has the small bowel lost surface area because of atrophy, inflammation, or surgical removal? Is the gut edematous because of hypoalbuminemia or congestive heart failure? Is bowel motility impaired by opioids, anticholinergics, or mechanical ileus? Is digestion limited by pancreatic or bile acid insufficiency? Has absorption been decreased by intestinal ischemia or gastrointestinal bleeding? Decreased surface area, bowel edema, and diminished digestive juices are only partial losses of small bowel function. An elemental formula should be tried first in these situations. Any of the other problems alone or in combination probably preclude the use of the small bowel and the patient will need total parenteral nutrition. If gastrointestinal function is adequate, then other organ failures that result in specific nutrient intolerance must be ruled out. If gastrointestinal function is adequate and no other organ failures preclude the use of a polymeric formula, then one must decide if stress and hypermetabolism are present. Enteral feeding is the preferred method of providing specialized nutrition support. Bowel rest reduces the barrier functions of the gut and malnutrition reduces cell-mediated immunity. The indications and relative contraindications for enteral tube feeding are also reviewed. The rationale for the formula design and the evidence for formula efficacy are presented. Polymeric, elemental, organ-specific, and immune-modulating formulas are discussed. Guidelines for formula selection are suggested.

Enteral Nutrition↗

PubMed1980

The mechanism of Na+-dependent D-glucose transport.

The mechanism of Na+-dependent D-glucose transport was investigated by kinetic means in rabbit small intestinal and renal brush border membranes. The rate of glucose transport was measured under equilibrium exchange conditions as a function of its own concentration and of the Na+ concentration. Likewise, the rate of Na+ transport was measured as a function of the D-glucose concentration. Noteworthy characteristics of the Na+-dependent glucose transport system are: 1) linear dependence of the glucose transport rate on Na+ concentration up to 0.1 M (at constant ionic strength), indicating a 1:1 stoichiometry of Na+-D-glucose cotransport under net flux conditions; 2) virtual Na+ independence of the apparent affinity of the transport system for D-glucose; 3) a stimulation-inhibition pattern if the transport rate of either substrate (D-glucose, Na+) is measured as function of increasing concentrations of its co-substrate; 4) a varying flux ratio of D-glucose to Na+ which can be either above or below 1, depending on the concentration ratio of the two substrates; 5) a rate constant for translocation of the loaded carrier which is faster than that for the dissociation of Na+. Treating Na+-D glucose co-transport analogous to an enzyme reaction, these features are consistent with an iso-ordered-bi-bi kinetic model, whereby the first solute that binds to the transport system at one membrane interface is the one that is released first at the other interface (first-in-first-out characteristics). The kinetic model is explained by a gated pore mechanism, whereby the translocation of the transported solutes across the permeability barrier is achieved by a rocker-type conformational change of the transport system (presumed to be a protein) which moves the permeability barrier past the solutes.

Animals↗

PubMed2005

Role of N-terminal amino acids in the absorption-enhancing effects of the c-terminal fragment of Clostridium perfringens enterotoxin.

We recently found that a polypeptide, the C-terminal of Clostridium perfringens enterotoxin (C-CPE), was a novel type of drug absorption enhancer. The C-terminal of C-CPE is thought to play a role in the binding of C-CPE to its receptor, claudin-4; however, the function of the N-terminal of C-CPE is unclear. In the present study, we evaluated the role of the N-terminal domain of C-CPE in jejunal absorption and claudin-4 binding. The treatment of rat jejunum with C-CPE resulted in enhanced absorption of dextran, with a molecular weight of 4000 Da. However, treatment with C-CPE220, which lacks the 36 N-terminal amino acids of C-CPE, did not enhance jejunal absorption. C-CPE had affinity for claudin-4 in rat jejunum lysates and Caco-2 lysates, but C-CPE220 did not. Interaction of C-CPE with the recombinant extracellular domain 2 of human claudin-4 (EC2hCld-4), which is the putative binding site for C-CPE, was observed, but C-CPE220 had no affinity for EC2hCld-4. To investigate the effect of C-CPE220 on the barrier function of tight junctions, we measured transepithelial electric resistance (TER) in C-CPE- or C-CPE220-treated Caco-2 monolayer cells. Although C-CPE decreased TER in Caco-2 monolayer cells, C-CPE220 did not disrupt the barrier function of tight junctions. Together, these results indicate that the 36 N-terminal amino acids of C-CPE may be necessary for the enhanced absorption mediated by C-CPE and play a partial role in binding to claudin-4.

Amino Acid Sequence↗

PubMed2003

Role of enteric glial cells in inflammatory bowel disease.

Enteric glial cells (EGCs) represent an extensive but relatively poorly described cell population within the gastrointestinal tract. Accumulating data suggest that EGCs represent the morphological and functional equivalent of CNS astrocytes within the enteric nervous system (ENS). The EGC network has trophic and protective functions toward enteric neurons and is fully implicated in the integration and the modulation of neuronal activities. Moreover, EGCs seem to be active elements of the ENS during intestinal inflammatory and immune responses, sharing with astrocytes the ability to act as antigen-presenting cells and interacting with the mucosal immune system via the expression of cytokines and cytokine receptors. Transgenic mouse systems have demonstrated that specific ablation of EGC by chemical ablation or autoimmune T-cell targeting induces an intestinal pathology that shows similarities to the early intestinal immunopathology of Crohn's disease. EGCs may also share with astrocytes the ability to regulate tissue integrity, thereby postulating that similar interactions to those observed for the blood-brain barrier may also be partly responsible for regulating mucosal and vascular permeability in the gastrointestinal tract. Disruption of the EGC network in Crohn's disease patients may represent one possible cause for the enhanced mucosal permeability state and vascular dysfunction that are thought to favor mucosal inflammation.

Animals↗

PubMed2005

Gene expression changes reveal patterns of aging in the rat digestive tract.

Similarly to other organs, the human digestive system is adversely affected by aging presenting physiologic manifestations that include compromised absorption and secretion, decreased motility, weakened mucosal barrier and as well as a high incidence of colon cancer. As biomedical advances enable the population to live longer, our understanding of molecular events that govern aging and disease states is enhanced through methodical analyses of temporal tissue-specific gene expression profiles. Recently, DNA microarray analyses have been employed to examine age-associated transcriptional profiles in the mammalian digestive tract. Gene expression patterns revealed that the magnitude and trend of age-associated changes differ in the rat colon and duodenum. Interestingly, the expression of genes involved in energy-generating metabolic pathways was decreased in the duodenum and increased in the colon. Microarray analyses detected modulations in expression of genes associated with compromised intestinal function and propensity for colon cancer in the aged population. Furthermore, altered expression was observed for certain genes implicated in governance of aging and lifespan in other organisms suggesting intriguing commonalities across species. Thus, these studies demonstrated feasibility and usefulness of DNA microarrays for identifying pathways involved in the molecular pathophysiology of the aging process and lifespan control in complex organisms.

Aging↗

PubMed1999

Domperidone: a peripherally acting dopamine2-receptor antagonist.

OBJECTIVE: To review the pharmacology, pharmacokinetics, efficacy, and safety of domperidone in the treatment of gastrointestinal motility disorders and emesis. DATA SOURCES: MEDLINE and Excerpta Medica online databases were searched to identify published reports. STUDY SELECTION: Domperidone has been marketed worldwide outside the US since 1978, and extensive clinical data for this drug are available. This review focuses on the clinical experience from controlled studies of domperidone in the treatment of motility disorders, particularly diabetic gastroparesis. Also, case reports are used in summarizing safety. The control comparator groups included placebo or other prokinetic drugs (metoclopramide and cisapride). Controlled clinical trials of domperidone's efficacy and safety as an antiemetic are also briefly examined. Although a variety of domperidone dosage forms have been marketed, data generated from trials using the 10-mg tablet are highlighted because this is the only dosage form available in Canada and is under investigation in the US. DATA EXTRACTION: Because symptoms do not correlate with objective measures of gastrointestinal motility and they are the primary reason that patients with motility disorders seek treatment, the primary outcome extracted from the clinical studies was symptomatic response to treatment. Safety and efficacy between domperidone and placebo, metoclopramide, or cisapride were compared. DATA SYNTHESIS: Domperidone, a peripheral dopamine2-receptor antagonist, regulates the motility of gastric and small intestinal smooth muscle and has been shown to have some effects on the motor function of the esophagus. It also has antiemetic activity as a result of blockade of dopamine receptors in the chemoreceptor trigger zone. In controlled clinical trials, domperidone provided better relief of symptoms (anorexia, nausea, vomiting, abdominal pain, early satiety, bloating, distension) than placebo in patients with symptoms of diabetic gastropathy; symptomatic improvement was similar with domperidone and metoclopramide or cisapride. Domperidone also provided short-term relief of symptoms in patients with dyspepsia or gastroesophageal reflux, prevented nausea and vomiting associated with emetogenic chemotherapy, and prevented the gastrointestinal and emetic adverse effects of antiparkinsonian drugs. Because very little domperidone crosses the blood-brain barrier, reports of central nervous system adverse effects, such as dystonic reactions, are rare. CONCLUSIONS: Domperidone is a unique gastrokinetic and antiemetic drug. Because of its favorable safety profile, domperidone appears to be an attractive alternative to metoclopramide. In the management of diabetic gastropathy, domperidone's antiemetic activity distinguishes it from cisapride.

Animals↗

PubMed1997

Mucosal permeability changes during intestinal reperfusion injury. The role of mast cells.

The objective of this study was to investigate the role of intestinal mast cells in mucosal functional and morphological alterations induced by 30 min segmental ischemia and 120 min reperfusion in anesthetized dogs. The time course of permeability changes of the mucosa to sodium fluorescein (NaFl) in blood-lumen and lumen-blood directions was studied in two separate series of experiments. Local hemodynamics, intramucosal pH (pHi) alterations, mast cell number and degranulation and the degree of tissue injury were determined. The effects of cromolyn (peritoneal-type mast cell stabilizer), quercetin (mucosal-type mast cell stabilizer), and dexamethasone (aspecific membrane stabilizer and mast cell depleter) pretreatments were evaluated. Ischemia-reperfusion induced significant tissue injury, elevated segmental vascular resistance, and decreased pHi. The blood to lumen clearance of NaFl increased significantly during ischemia and reperfusion. Cromolyn and quercetin pretreatment significantly inhibited permeability changes, but did not influence pHi and morphological alterations induced by ischemia-reperfusion. Dexamethasone pretreatment did not influence the number of mast cells, however, the degree of mast cell degranulation and the degree of mucosal damage decreased. These results demonstrate that mast cells or mast cell-induced reactions contribute to the mucosal permeability alterations and barrier lesions during reperfusion, but play a minor role in reperfusion-induced structural injury.

Animals↗

PubMed1990

Pathophysiology and pharmacokinetics following burn injury.

Therapy for inpatient burn victims is a clear challenge for the clinician, since directly following injury the pharmacokinetic parameters of many drugs will change drastically. Blood flow to the tissues is decreased; the rate of distribution and elimination of intravenous drugs administered during this time is reduced, and absorption of oral drugs may be slowed. Approximately 48 hours after injury, the blood flow increases, as does internal core temperature; the rates may increase as a result. Immediately after injury, plasma albumin level rapidly decreases and remains significantly depressed even at 60 days post-burn. Thus, the protein binding of acidic and neutral drugs will decrease and higher amounts of free fraction will be available at the biophase. On the other hand, alpha 1-acid glycoprotein increases in concentration and remains elevated at least 20 days post-burn. Basic drugs exhibit increased protein binding and will most probably need an increased dosage to achieve the appropriate pharmacological effect. Hepatic metabolism is also affected: the rate of phase I metabolism will decrease while phase II metabolism is unimpaired and may possibly increase. Other liver functions, such as protein synthesis, are also impaired. The effect on phase I drug metabolism is believed to be due to oxygen-derived free radicals released during the course of injury. In those patients with full-thickness burns, the epidermal layer is destroyed. Topical drugs have less of a barrier to cross and, consequently, less drug is needed to achieve effectiveness. In addition, the stomach has been found to secrete excess protons which will eventually lead to ulcers in the majority of patients. Hyperchlorhydria may affect the dissolution and disintegration of orally administered drugs in tablet form, as well as the partitioning of the neutral un-ionised species between the stomach and bloodstream. In the small intestine decreased nutrient absorption and DNA synthesis occurs, but the effect this may have on drug absorption is questionable. This paper focuses on the epidemiology of burn injuries and the way in which the pathophysiology following such injury alters the pharmacokinetics of a drug. Specific examples are provided. Some mention is made of burn management, therapeutic drug monitoring in burn patients, experimental design considerations, and future research topics.

Animals↗

PubMed2006

Microarray analysis of human epithelial cell responses to bacterial interaction.

Host-pathogen interactions are inherently complex and dynamic. The recent use of human microarrays has been invaluable to monitor the effects of various bacterial and viral pathogens upon host cell gene expression programs. This methodology has allowed the host response transcriptome of several cell lines to be studied on a global scale. To this point, the great majority of reports have focused on the response of immune cells, including macrophages and dendritic cells. These studies revealed that the immune response to microbial pathogens is tailored to different microbial challenges. Conversely, the paradigm for epithelial cells has--until recently--held that the epithelium mostly served as a relatively passive physical barrier to infection. It is now generally accepted that the epithelial barrier contributes more actively to signaling events in the immune response. In light of this shift, this review will compare transcriptional profiling data from studies that involved host-pathogen interactions occurring with epithelial cells. Experiments that defined both a common core response, as well as pathogen-specific host responses will be discussed. This review will also summarize the contributions that transcriptional profiling analysis has made to our understanding of bacterial physio-pathogensis of infection. This will include a discussion of how host transcriptional responses can be used to infer the function of virulence determinants from bacterial pathogens interacting with epithelial mucosa. In particular, we will expand upon the lessons that have been learned from gastro-intestinal and oral pathogens, as well as from members of the commensal flora.

Animals↗

PubMed1994

Receptor-mediated transport of therapeutics across the blood-brain barrier.

The delivery of nonlipophilic compounds to the brain is severely hindered by the blood-brain barrier (BBB). However, brain capillary endothelial cells, which form the BBB, do possess specific receptor-mediated transport mechanisms that potentially can be exploited as a means to transport therapeutic molecules to the brain. We have found that antibodies that bind to the transferrin receptor selectively target BBB endothelium, are transported into the brain, and can function as carriers for the delivery of compounds, including proteins, to the central nervous system. This drug delivery system has been used to transport nerve growth factor across the BBB in a biologically active form and at levels sufficient to prevent the degeneration of nerve growth factor-dependent neurons.

Animals↗

PubMed1988

Tissue population configuration as a modifier of organ dose response.

Organ tissue populations exist in different spatial configurations. There are the idealized "volume" configuration (bone marrow), the "monolayer" (skin basal cell or large vessel endothelial populations), the "linear" (microvascular endothelial populations) and the "isolated unit" (capillaries, intestinal crypt). This defines the size of the irradiated population (No) and influences the absolute number of cells (N) that survive per unit of tissue dimension to permit repopulation. A proliferative cell that survives irradiation replaces cells lost from distant locations according to its spatial dimension. However, in the isolated unit configuration, a proliferative cell can replace those cells lost from the unit, but an anatomical barrier prevents cell replacement extending to adjacent units. Recovery of a tissue following irradiation depends not only on the number of surviving proliferative cells, but also on the organization of those cells into sub-populations. A regenerative unit is a subpopulation capable of being regenerated from the survival of a single cell. A tissue "functional unit" is a subcomponent of the tissue which contributes independently to overall tissue function, and whose loss results in an irreversible incremental loss of function. Survival of the functional unit depends critically on the degree of interdependence among component regenerative units, and such interdependence is strongly influenced by the tissue's spatial organization. Using these concepts, a mathematical formulation expresses a tissue's functional response to irradiation in terms of cell survival parameters, the spatially-related parameters of regenerative unit size, and the number of interdependent regenerative units comprising a functional unit. It is argued that this provides a more realistic approach toward simulating the radiation response of an organ than one based on tissue bulk cell survival parameters alone.

Cell Division↗

PubMed1994

Mononuclear cells from infants allergic to cow's milk secrete tumor necrosis factor alpha, altering intestinal function.

BACKGROUND/AIMS: Intestinal dysfunction observed during cow's milk allergy (CMA) is incompletely understood, and neither the effector cells nor the mediators responsible have been clearly identified. This study was undertaken to better characterize the implication of mononuclear cells in food allergy. METHODS: Peripheral blood mononuclear cells (PBMC) from infants with CMA were cultured in the presence of cow's milk proteins (CMP), and the release of tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), and interleukin 4 and 6 was measured. The effect of culture supernatants was tested on HT29 cl.19A intestinal cell monolayers mounted in Ussing chambers. RESULTS: When stimulated by CMP, PBMC from infants with CMA released more TNF-alpha than those from control infants (429 +/- 92 vs. 205 +/- 34 pg/mL). Culture supernatants did not directly stimulate electrogenic chloride secretion by HT29 cl.19A cells, but epithelial barrier capacity was altered as shown by the significant decrease in electrical resistance (85 +/- 17 vs. 135 +/- 14 omega.cm2 in controls) and the increases in intact horseradish peroxidase, [14C]mannitol, and 22Na+ fluxes. These effects were reversed when culture supernatants were neutralized with anti-TNF-alpha antibodies. Recombinant human-TNF-alpha altered the HT29 cl.19A epithelial barrier capacity, and its effect was highly potentiated by IFN-gamma. CONCLUSIONS: These results indicate that during CMA, the high level of TNF-alpha released by mononuclear cells after milk protein challenge acts synergistically with IFN-gamma to increase the intestinal permeability.

Cell Line↗

PubMed2005

Probiotic therapy of intestinal inflammation and infections.

PURPOSE OF REVIEW: The author presents evidence published during the past year regarding treatment of clinical and experimental intestinal inflammation and infections by probiotic agents. RECENT FINDINGS: Normal commensal bacteria are implicated in the pathogenesis of chronic, immune-mediated intestinal inflammation, particularly Crohn disease and pouchitis, whereas viral, bacterial, fungal, and protozoan infections are increasingly important with widespread use of immunosuppressive agents and broad-spectrum antibiotics. Combinations of Lactobacilli, Bifidobacteria, and Streptococcus salivarius prevent relapse of recurrent pouchitis and perhaps decrease the initial onset of pouch inflammation, whereas Escherichia coli Nissle 1917 maintains remission in ulcerative colitis. Several agents offer promise as primary therapy of ulcerative colitis. Use of probiotics in Crohn disease remains unsubstantiated. Animal models demonstrate marked differences in responses among various probiotic bacterial species and that nonviable organisms can have therapeutic efficacy. Probiotics have multiple mechanisms of action, including prevention of pathogenic bacterial growth, binding to or penetration of pathogens to mucosal surfaces, stimulation of mucosal barrier function, or altering immunoregulation (decreasing proinflammatory and promoting protective molecules). Although multiple probiotic species block epithelial adhesion and invasion by microbial pathogens in vitro, their proven utility in clinical infections is limited to accelerating recovery from acute infectious diarrhea and preventing antibiotic-associated diarrhea. SUMMARY: Probiotics offer promise for physiologic, nontoxic treatment of pouchitis, ulcerative colitis, and acute infectious diarrhea, but larger, controlled clinical studies must be performed to clarify optimal agents; doses; combinations of various probiotics, prebiotics, and antibiotics; and therapeutic conditions.

Animals↗

PubMed1987

[Contribution of radiology in the study of ileal reservoirs anastomosed to the anal canal].

Confection of an ileal reservoir anastomosed to anal canal is a seductive issue after total coloproctectomy. In this prospective study, early complications, mainly anastomotic fistulae, were effectively detected by routine enemas with water soluble media. These complications affected 14% of patients. Preliminary results of functional exploration of reservoirs by defecography showed that continence muscle barriers were apparently unaltered by the operation, that the content of reservoirs in J was satisfactory and that difficulties in exoneration frequently met with in reservoirs in S were due to architectural anomalies of these ileal pouches rather than a disturbance in pelvic muscles play. Radiologic analysis can establish perfection of surgical mounting and guide possible recovery operations.

Adolescent↗