Prebiotics and mucosal barrier function.
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Dietary Fiber↗
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Breast milk and the prevention of neonatal and preterm gastrointestinal disease states: a new perspective.
In this review of the protective properties of human breast milk, a new perspective is taken to underscore the passive and active protection properties of breast milk in providing specific protection against selective gastrointestinal disease affecting the neonate and preterm infant. The normal protective properties of the gastrointestinal epithelial barrier (immunologic and nonimmunologic) are considered as is the development of barriers to antigen absorption in the immature infant human intestine as a background for considering three accelerated gastrointestinal diseases-necrotizing enterocolitis, intestinal allergy, and bacterial gastroenteritis. In each of these conditions, the developmental protective defect is considered and the role of breast milk plays in filling the protective void discussed. Besides considering passive protection of breast milk including the new roles assigned to nutrients such as lactoferrin and nucleotides, and importance of active substances in breast milk such as growth factors, cytokines and hormones are discussed in the context of actively stimulating the infant's own intestinal defenses to function as a protective barrier. Future studies at the cellular and molecular level should be helpful in designing both preventative and treatment strategies to deal with these diseases.
Female↗
The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure.
Traditionally, evaluation of intestinal function has been limited largely to monitoring gastric pH and intestinal motility. This clinical approach has led clinicians to equate normal intestinal motility with normal intestinal function and to assume that if stress-induced gastric bleeding can be prevented, all will be well. However, it is becoming increasingly clear that the gastrointestinal tract is not a passive organ and that intestinal dysfunction is not limited to ileus and upper gastrointestinal bleeding. Instead, the gastrointestinal tract is recognized as having important endocrine, metabolic, immunologic, and barrier functions, as well as its traditional role in nutrient absorption. Over the last 5 years, there has been a resurgence of interest in the role of intestinal barrier failure in the development of systemic infection and multiple organ failure in the critically ill or injured patient.
Bacteria↗
Probiotics and gut inflammation.
The intestine's mucosal surface provides a defense barrier against antigens encountered by the enteric route. In this system a balance is generated and maintained between host and microfloral bacteria. In intestinal inflammation, the integrity of the barrier is disrupted, a greater amount of antigens traverses the mucosal barrier, and the routes of transport are altered, possibly evoking aberrant immune responses and release of proinflammatory cytokines with further impairment of the barrier function. Nutritional therapy remains an attractive tool in the management of intestinal inflammation. The advances this past year are related to the ecologic system provided by specific strains of gut microflora, the concept of healthy microflora, and ways in which gut barrier function could be strengthened by consumption of mono-and mixed cultures of beneficial live microorganisms as probiotics.
Journal Article↗
Pharmacokinetic examination of antipyrine passage through the placenta and the small intestine in rats.
The placental and small intestinal barriers, though obviously different, show many functional as well as morphological similarities. When the surface area of both barriers in man was recalculated to a unit of body weight, nearly identical values (2.71 and 2.86 m2/kg of body mass, respectively) were obtained. The aims of the present study were (1) to compare mutual permeability of these two barriers to antipyrine (AP), and (2) to describe pharmacokinetics of AP in pregnant and non-pregnant rats. In placental studies AP showed that its rapid transfer through the placenta (k(tr) = 0.046 min(-1)) was governed by the mechanism of passive diffusion. In the closed circuit, FMCR(eq) was 1.085, t(eq) was 112.10 min and k(eq) was 0.020 min(-1). Absorptive studies performed on the rat small intestine indicated an identical mechanism of drug transport. The apparent first-order absorption rate constant of AP was 0.479 min(-1), and Tmax was 8.95 minutes. Differences in AP pharmacokinetics between pregnant and non-pregnant rats were significant during the distribution phase (t(1/2) = 3.78 and 5.87 min, respectively), whereas the elimination phase was unaffected. AP has been demonstrated, as expected, to be an excellent marker for drug transport studies through different body barriers.
Animals↗
Boosted systemic immune and local responsiveness after intestinal inflammation in orally sensitized guinea pigs.
BACKGROUND & AIMS: Intestinal inflammation resulting in disruption of the mucosal barrier function has been proposed as a cause of increased incidence of allergic diseases. This study was designed to evaluate whether intestinal inflammation is able to change the immune responsiveness to sensitization and antigen challenge responses. METHODS: Guinea pigs orally sensitized to cow's milk proteins were either treated or not treated with trinitrobenzenesulfonic acid (TNBS) to induce intestinal inflammation and compared with control animals (not sensitized). Systemic immune and local responsiveness to antigen challenge were assessed by measuring antibody serum titers, colonic fluid secretion, mucosal histamine level, and mucus depletion. Intestinal permeability was evaluated from 51Cr-ethylenediaminetetraacetic acid (EDTA) recovery and beta-lactoglobulin serum level. RESULTS: Immunoglobulin E titers were higher in TNBS-treated animals than in non-TNBS-treated sensitized animals. Antigen challenge in TNBS-treated animals induced a fourfold increase of colonic secretion and greater histamine and mucus depletion than in non-TNBS-treated animals. Permeability to 51Cr-EDTA increased 5 days after TNBS treatment but was unchanged after antigen challenge. In contrast to controls, beta-lactoglobulin was not detected in the sera of challenged sensitized and TNBS-treated animals. CONCLUSIONS: Intestinal inflammation increasing gut permeability enhances the sensitization process. Therefore, local anaphylactic reactions are exacerbated after antigen challenge.
Analysis of Variance↗
Development of immune function in the intestine and its role in neonatal diseases.
This review has traced the ontogeny of the human mucosal immune system, speculating that appropriate gut immune responses are essential in preventing many significant neonatal enteric diseases. Because the gastrointestinal tract serves as the portal of entry for many potential antigens, its mucosal immune function is essential in controlling antigenic responses and ensuring systemic tolerance. A thorough under standing of the development of the entire immune system is essential in defining intestinal mucosal immune function. From the protective barrier covering the enterocyte to the intraepithelial T lymphocytes, these components work together to limit antigen passage from the gut lumen to the underlying immune cells and, thus, promote normal immunity and tolerance. When abnormalities exist or when this immune barrier has not matured fully, conditions afflicting newborns, especially preterm infants, occur. Necrotizing enterocolitis, milk-protein enteropathy, and enteric bacterial infections are only three clinical examples of how aberrant gut immune-mediated defenses may have a significant role in their pathogenesis. In clinical practice, it is not only important to recognize these conditions at their onset but also to understand the basis for the underlying illness and identify newborns who are at an increased risk of acquiring them.
Bacterial Adhesion↗
Inducible nitric oxide synthase gene knockout mice have increased resistance to gut injury and bacterial translocation after an intestinal ischemia-reperfusion injury.
OBJECTIVE: Intestinal ischemia-reperfusion after severe shock states is often associated with bacterial translocation and intestinal barrier dysfunction. Our previous studies showed that inducible nitric oxide synthase (iNOS) gene knockout mice were resistant to endotoxin-induced bacterial translocation and ileal mucosal damage. The goal of this study was to test whether iNOS mediates bacterial translocation after intestinal ischemia-reperfusion, using iNOS knockout mice (iNOS-/-) and their wild-type littermates (iNOS+/+). DESIGN: Prospective animal study with concurrent controls. SETTING: Small animal laboratory. SUBJECTS: Thirty-eight iNOS knockout mice and 51 wild-type littermates. INTERVENTIONS: iNOS+/+ mice or iNOS-/- mice were subjected to a sham operation or 30 mins of superior mesenteric artery occlusion followed by reperfusion. Twenty-four hours after reperfusion, bacterial translocation to mesenteric lymph nodes, ileal villous damage, and cecal bacterial population were evaluated. MEASUREMENTS AND MAIN RESULTS: Sham operation did not induce bacterial translocation, change cecal bacterial population levels, or cause ileal villous damage. Intestinal ischemia-reperfusion caused bacterial translocation in 72% of the iNOS+/+ mice but only 28% of the iNOS-/- mice. Both iNOS+/+ and iNOS-/- mice subjected to superior mesenteric artery occlusion (SMAO) in which bacterial translocation occurred had cecal bacterial population levels that were three logs higher than mice subjected to sham SMAO or mice subjected to SMAO in which bacterial translocation did not occur. The magnitude of villous injury was less in the iNOS-/- mice than the iNOS+/+ mice after SMAO, although the incidence of ileal villous damage was significantly higher in both the iNOS+/+ and iNOS-/- mice in which bacterial translocation occurred after SMAO than in the mice in which bacterial translocation did not occur after SMAO. iNOS+/+ mice subjected to SMAO had increased plasma concentrations of nitrite (NO2-) and nitrate (NO3-), and the plasma concentrations of NO2- and NO3- were highest in the mice in which bacterial translocation had occurred. CONCLUSION: iNOS knockout mice were more resistant to intestinal ischemia-reperfusion-induced bacterial translocation and mucosal injury than wild-type mice, suggesting that iNOS might play a role in intestinal ischemia-reperfusion-induced loss of gut barrier function.
Animals↗
Functional and morphological changes of the gut barrier during the restitution process after hemorrhagic shock.
AIM: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response to ischemia/reperfusion injury. METHODS: Forty-seven Sprague-Dawley rats with body weight of 250-300 g were divided into two groups: control group (sham shock n = 5) and experimental group (n = 42). Experimental group was further divided into six groups (n = 7 each) according to different time points after the hemorrhagic shock, including 0(th) h group, 1st h group, 3rd h group, 6th h group, 12th h group and 24th h group. All the rats were gavaged with 2 mL of suspension of lactulose (L) (100 mg/2 mL) and mannitol (M) (50 mg/each) at the beginning and then an experimental rat model of hemorrhagic shock was set up. The specimens from jejunum, ileum and colon tissues and the blood samples from the portal vein were taken at 0, 1, 3, 6, 12 and 24 h after shock resuscitation, respectively. The morphological changes of the intestinal mucosa, including the histology of intestinal mucosa, the thickness of mucosa, the height of villi, the index of mucosal damage and the numbers of goblet cells, were determined by light microscope and/or electron microscope. The concentrations of the bacterial endotoxin lipopolysaccharides (LPS) from the portal vein blood, which reflected the gut barrier function, were examined by using Limulus test. At the same time point, to evaluate intestinal permeability, all urine was collected and the concentrations of the metabolically inactive markers such as L and M in urine were measured by using GC-9A gas chromatographic instrument. RESULTS: After the hemorrhagic shock, the mucosal epithelial injury was obvious in small intestine even at the 0(th) h, and it became more serious at the 1st and the 3rd h. The tissue restitution was also found after 3 h, though the injury was still serious. Most of the injured mucosal restitution was established after 6 h and completed in 24 h. Two distinct models of cell death-apoptosis and necrosis-were involved in the destruction of rat intestinal epithelial cells. The number of goblet cells on intestinal mucosa was reduced significantly from 0 to 24 h (the number from 243+/-13 to 157+/-9 for ileum, 310+/-19 to 248+/-18 for colon; r = -0.910 and -0.437 respectively, all P<0.001), which was the same with the large intestine, but the grade of injury was lighter with the values of mucosal damage index in 3 h for jejunum, ileum, and colon being 2.8, 2.6, 1.2, respectively. The mucosal thickness and the height of villi in jejunum and ileum diminished in 1 h (the average height decreased from 309+/-24 to 204+/-23 microm and 271+/-31 to 231+/-28 microm, r = -0.758 and -0.659, all P<0.001; the thickness from 547+/-23 to 418+/-28 microm and 483+/-45 to 364+/-35 microm, r = -0.898 and -0.829, all P<0.001), but there was no statistical difference in the colon (F = 0.296, P = 0.934). Compared with control group, the urine L/M ratio and the blood LPS concentration in the experimental groups raised significantly, reaching the peak in 3-6 h (L/M: control vs 3 h vs 6 h was 0.029+/-0.09 vs 0.063+/-0.012 vs 0.078+/-0.021, r = -0.786, P<0.001; LPS: control vs 3 h vs 6 h was 0.09+/-0.021 vs 0.063+/-0.012 vs 0.25+/-0.023, r = -0.623, P<0.001), and it kept increasing in 24 h. CONCLUSION: The gut barrier of the rats was seriously damaged at the early phase of ischemic reperfusion injury after hemorrhagic shock, which included the injury and atrophy in intestinal mucosa and the increasing of intestinal permeability. Simultaneously, the intestinal mucosa also showed its great repairing potentiality, such as the improvement of the intestinal permeability and the recovery of the morphology at different phases after ischemic reperfusion injury. The restitution of gut barrier function was obviously slower than that of the morphology and there was no direct correlation between them. Compared with the small intestine, the large intestine had stronger potentiality against injury. The reduction of the amount of intestinal goblet cells by injury did not influence the ability of intestinal mucosal restitution at a certain extent and it appeared to be intimately involved in the restitution of the epithelium.
Animals↗
Absorption of albumin by the midgut of a lepidopteran larva.
In the last decade, the study of peptide and protein absorption by the insect gut has received increasing attention because of the considerable impact this information may have on the development of new delivery strategies for insecticide macromolecules targeting haemocoelic receptors. Available experimental evidence in vivo suggests that, in insects, peptides and proteins can cross the intestinal barrier reaching the haemocoel, but the functional bases of this absorption pathway have not yet been thoroughly investigated. The current knowledge of the mechanisms involved in protein and polypeptide absorption in animals derives from the extensive studies performed in mammalian polarised epithelial cells, where the transcellular transport of proteins by transcytosis has been demonstrated. In this process, proteins are internalised at one pole of the cell and transported by cytoplasmic vesicular traffic to the opposite plasma membrane domain, where they are released with unchanged biological activity. Here we report data on albumin translocation across the isolated midgut of Bombyx mori caterpillars perfused in vitro. The functional properties of the transepithelial transport of this protein are described and, since absorption prevails over secretion, its lumen-to-haemolymph flux is characterised. Low-temperature incubations nearly abolish the transepithelial transport, while the peculiar physiological features of the larval midgut, i.e. the high lumen positive transepithelial voltage and the luminal alkaline pH, do not affect the flux. The obtained results indicate that albumin crosses B. mori larval midgut by transcytosis.
Albumins↗
[HIV enteropathy].
HIV enteropathy is defined, according to authors, by intestinal histological anomalies presumed to be induced by HIV and/or the chronic diarrhea of AIDS progressing in the absence of any detectable intestinal infectious pathogen. HIV can certainly infect the mononuclear cells of the chorion of the intestinal mucosa, and probably certain colonocytes. The links between infection of these cells and HIV enteropathy remain very poorly understood. Certain authors attribute a preponderant role to possible abnormalities of enterocyte renewal induced by HIV, and others to intestinal mucosal inflammation induced by the infection and activation of lymphocytes of the mucosal chorion. Multifactorial, anatomical and functional, involvement of the mucosal barrier of the entire intestine is no doubt closest to the truth.
CD4-Positive T-Lymphocytes↗
Induction of a rat enteric defensin gene by hemorrhagic shock.
Multicellular organisms utilize a battery of extracellular and cellular mechanisms to defend against microbial infiltration. Among the armamentarium used by the small intestine to defend against microbial invasion are antimicrobial peptides called defensins. We previously have shown that gut barrier function is impaired following hemorrhagic shock, resulting in translocation of bacteria or endotoxin. Using a rat model, we examined the effect of hemorrhagic shock on alpha-defensin expression. We utilized the anchored reverse transcriptase PCR strategy to isolate a rat enteric defensin cDNA. The cDNA is 406 bases in length and encodes a putative prepro-enteric defensin that we have named rat defensin 5 (RD-5). RD-5 expression is restricted to the small intestine and is specifically localized by in situ hybridization to the Paneth cells. A 10-fold increase in its steady state levels was observed in the distal intestine immediately after the termination of shock. This is the first study to show that enteric defensins are inducible following injury. We suggest that enteric defensins may contribute to the complex and integrated barrier function of the intestinal mucosal surface.
Amino Acid Sequence↗
Recovery of mucosal barrier function in ischemic porcine ileum and colon is stimulated by a novel agonist of the ClC-2 chloride channel, lubiprostone.
Previous studies utilizing an ex vivo porcine model of intestinal ischemic injury demonstrated that prostaglandin (PG)E(2) stimulates repair of mucosal barrier function via a mechanism involving Cl(-) secretion and reductions in paracellular permeability. Further experiments revealed that the signaling mechanism for PGE(2)-induced mucosal recovery was mediated via type-2 Cl(-) channels (ClC-2). Therefore, the objective of the present study was to directly investigate the role of ClC-2 in mucosal repair by evaluating mucosal recovery in ischemia-injured intestinal mucosa treated with the selective ClC-2 agonist lubiprostone. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers, and short-circuit current (I(sc)) and transepithelial electrical resistance (TER) were measured in response to lubiprostone. Application of 0.01-1 microM lubiprostone to ischemia-injured mucosa induced concentration-dependent increases in TER, with 1 microM lubiprostone stimulating a twofold increase in TER (DeltaTER = 26 Omega.cm(2); P < 0.01). However, lubiprostone (1 microM) stimulated higher elevations in TER despite lower I(sc) responses compared with the nonselective secretory agonist PGE(2) (1 microM). Furthermore, lubiprostone significantly (P < 0.05) reduced mucosal-to-serosal fluxes of (3)H-labeled mannitol to levels comparable to those of normal control tissues and restored occludin localization to tight junctions. Activation of ClC-2 with the selective agonist lubiprostone stimulated elevations in TER and reductions in mannitol flux in ischemia-injured intestine associated with structural changes in tight junctions. Prostones such as lubiprostone may provide a selective and novel pharmacological mechanism of accelerating recovery of acutely injured intestine compared with the nonselective action of prostaglandins such as PGE(2).
Alprostadil↗
Glutamine and barrier function in cultured Caco-2 epithelial cell monolayers.
Dietary glutamine (Gln) has been shown to be important for maintenance of the intestinal barrier. To investigate the role of the epithelium in this Gln dependence, Caco-2 cells were raised on semipermeable membranes under conditions that model different regions of the crypt and villus. Gln availability was controlled by addition to the medium and treatment with methionine sulfoximine to inhibit Gln synthetase (GS). Barrier function was assayed by measuring transepithelial electrical resistance and fluxes of [(14)C]mannitol and fluorescein isothiocyanate-dextran. The barrier function of these monolayers was found to require the Gln provided either in the medium at the apical or basal surface or via GS. However, the barrier was no more sensitive to Gln deprivation than it was to accumulation or maintenance of total protein. These results suggest that the in vivo dependence of the gut mucosal barrier on Gln likely involves roles separate from maintenance of the epithelial barrier per se.
Caco-2 Cells↗
Preventive and curative effects of probiotics in atopic patients.
Normally, the transport of allergens through the intestinal epithelia to the blood is limited. It is hypothesised that if these compounds arrive in the blood circulation, they must percolate through the epithelial cell layer. Thus, food allergy (and thus atopic eczema) implies an increased intercellular leakage of the gut wall. Such increased intercellular leakage is thought to be caused by a slightly changed cellular morphology due to a slight cytopathologic effect because of both a limited decay of the cytoskeleton and a slightly reduced turgor. These events may be due to a reduced production of intracellular metabolic energy in the epithelial cells due to an increased concentration of familiar, frequently occurring, potentially toxic bacterial metabolites, i.e., d-lactic acid and/or ethanol. In this hypothesis we suggest that adequate probiotics can (i) prevent the increased characteristic intestinal permeability of children with atopic eczema and food allergy, (ii) can thus prevent the uptake of allergens, and (iii) finally can prevent the expression of the atopic constitution. The use of adequate probiotic lactobacilli, i.e., homolactic and/or facultatively heterolactic l-lactic acid-producing lactobacilli, reduces the intestinal amounts of the bacterial, toxic metabolites, d-lactic acid and ethanol by fermentative production of merely the non-toxic l-lactic acid from glucose. Thus, it is thought that beneficial probiotic micro-organisms promote gut barrier function and both undo and prevent unfavourable intestinal micro-ecological alterations in allergic individuals.
Adult↗
Acute stressors stimulate ion secretion and increase epithelial permeability in rat intestine.
Wistar-Kyoto rats were subjected to 4 h restraint stress (RS) or cold restraint stress (CRS), and jejunal tissues were examined in Ussing chambers for alterations in transport functions compared with tissues from unstressed control rats. The baseline short-circuit current (Isc) was significantly elevated in tissues from RS (approximately 50%) and CRS (100%). Substitution of Cl- eliminated the abnormality, suggesting that stress stimulates Cl- secretion. Electrical transmural stimulation of enteric nerves caused a transient increase in Isc in all tissues. The magnitude of this response was significantly less in tissues from CRS than from control rats; however, the ability of the epithelium to secrete in response to exogenous stimulation with bethanechol or vasoactive intestinal polypeptide was unimpaired, implicating a neural change. Tissue conductance was higher in jejunum from RS and CRS rats than from controls. Increased intestinal epithelial permeability in stressed rats was confirmed by significantly greater fluxes of the inert radiolabeled probes, [3H]mannitol and 51Cr-labeled EDTA. No structural changes were observed. We conclude that acute stressors have profound effects on intestinal epithelial physiology, stimulating ion secretion and reducing barrier function.
Acute Disease↗
Expression of type 1 corticotropin-releasing factor receptor in the guinea pig enteric nervous system.
Reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, electrophysiological recording, and intraneuronal injection of the neuronal tracer biocytin were integrated in a study of the functional expression of corticotropin-releasing factor (CRF) receptors in the guinea pig enteric nervous system. RT-PCR revealed expression of CRF1 receptor mRNA, but not CRF2, in both myenteric and submucosal plexuses. Immunoreactivity for the CRF1 receptor was distributed widely in the myenteric plexus of the stomach and small and large intestine and in the submucosal plexus of the small and large intestine. CRF1 receptor immunoreactivity was coexpressed with calbindin, choline acetyltransferase, and substance P in the myenteric plexus. In the submucosal plexus, CRF1 receptor immunoreactivity was found in neurons that expressed calbindin, substance P, choline acetyltransferase, or neuropeptide Y. Application of CRF evoked slowly activating depolarizing responses associated with elevated excitability in both myenteric and submucosal neurons. Histological analysis of biocytin-filled neurons revealed that both uniaxonal neurons with S-type electrophysiological behavior and neurons with AH-type electrophysiological behavior and Dogiel II morphology responded to CRF. The CRF-evoked depolarizing responses were suppressed by the CRF1/CRF2 receptor antagonist astressin and the selective CRF1 receptor antagonist NBI27914 and were unaffected by the selective CRF2 receptor antagonist antisauvagine-30. The findings support the hypothesis that the CRF1 receptor mediates the excitatory actions of CRF on neurons in the enteric nervous system. Actions on enteric neurons might underlie the neural mechanisms by which stress-related release of CRF in the periphery alters intestinal propulsive motor function, mucosal secretion, and barrier functions.
Action Potentials↗
Influence of synbiotic containing Lactobacillus acidophilus La5, Bifidobacterium lactis Bb 12, Streptococcus thermophilus, Lactobacillus bulgaricus and oligofructose on gut barrier function and sepsis in critically ill patients: a randomised controlled trial.
BACKGROUND & AIMS: Infective complications are a common cause of mortality and morbidity in critically ill patients. Many factors affect sepsis, one of which is gut barrier function. The aim of this study was to determine whether the oral administration of a synbiotic preparation could alter gut barrier function in critically ill patients and thus reduce sepsis. METHODS: A total of 90 patients admitted to an intensive care unit (ICU) were randomised to receive either synbiotic or placebo preparations (45 into each group). The synbiotic preparation consisted of Lactobacillus acidophilus La5, Bifidobacterium lactis Bb 12, Streptococcus thermophilus and Lactobacillus bulgaricus (probiotics) with oligofructose (prebiotic). Gut barrier function was assessed by measurement of intestinal permeability (lactulose/rhamnose test) and culture of nasogastric aspirate on days 1 and 8. All septic complications and mortality were recorded. RESULTS: There were no differences between the groups in terms of age, sex, APACHE II or POSSUM scores. After 1 week of therapy, patients in the synbiotic group had a significantly lower incidence of potentially pathogenic bacteria (43% versus 75%, P = 0.05) and multiple organisms (39% versus 75%, P = 0.01) in their nasogastric aspirates than controls. There were no significant differences between the groups in terms of intestinal permeability, septic complications or mortality. CONCLUSIONS: The administration of synbiotic in critically ill patients favourably altered the microbial composition of the upper gastrointestinal tract but had no effect on intestinal permeability and was not associated with measurable clinical benefit.
Aged↗