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PubMed2004

[Copper treatment alters the barrier functions of human intestinal Caco-2 cells].

OBJECTIVE: To investigate the effects of copper on permeability and P-glycoprotein (P-gp) of Caco-2 cell monolayers. METHODS: The differentiated Caco-2 cell model was used in this study. Permeability of cell monolayers was reflected by monitoring transepithelial electrical resistance (TEER); distribution of tight junctional protein ZO-1 was measured by immunofluorescent staining; F actin was measured by fluorescence staining; and Activity of P-gp was reflected by changes of transcellular transport and accumulation of Rho-123 in Caco-2 cells. RESULTS: Apical treatment with copper (30 - 100 micromol/L, Hanks' buffered salt solution, up to 3 hours) induced a time- and concentration-dependent increase in permeability reflected by progressive decrease of TEER of Caco-2 cell monolayers, accompanied by deorganization of F actin, but without significant effects on tight junctional protein ZO-1; at a dose without any adverse effects on viability and permeability of Caco-2 monolayers, copper treatment (300 micromol/L, complete medium, 24 hours) decreased Papp(BL-->AP) from 7.37 +/- 0.20 x 10(-6) cm/s (controls) to (6.43 +/- 0.27) x 10(-6) cm/s, the increased Papp(AP-->BL) from (1.23 +/- 0.05) x 10(-7) cm/s (controls) to (3.41 +/- 0.08) x 10(-7) cm/s, and enhanced the intracellular Rho-123 from (0.31 +/- 0.01) nmol/filter (controls) to (0.50 +/- 0.03) nmol/filter. CONCLUSION: Copper might alter the barrier functions of Caco-2 cells through increasing the permeability and inhibiting P-gp of Caco-2 cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1981

Development of gastrointestinal mucosal barrier. II. The effect of natural versus artificial feeding on intestinal permeability to macromolecules.

We have recently reported that the intestinal transport of intact macromolecules into the circulation decreases with age presumably due to maturation of mucosal barrier factors. To extend this observation and determine the effect of natural versus artificial feeding on maturation of intestinal mucosal "barrier function" we conducted experiments which assessed both macromolecular transport and epithelial cell morphology. To study barrier function, we gavage fed a physiologic quantity (100 mg) of bovine serum albumin (BSA) to weight-matched breast- and bottle-fed infant rabbits at 1 and 2 wk of age and quantitated intestinal macromolecular transport by measuring circulating plasma concentrations of the intact antigen 4 hr later. a significant decrease (P less than 0.02) in immunoreactive bovine serum albumin (I-BSA) concentration was noted in breast-fed (6.12 +/- 0.77 micrograms I-BSA per ml plasma) compared with bottle-fed (9.19 +/- 0.93 micrograms I-BSA per ml plasma) animals at one wk. However, at 2 wk, no difference could be demonstrated between the two groups. Furthermore, small intestinal morphology evaluated by light and electron microscopy was similar in both groups each age. To determine if the lower plasma I-BSA noted at one wk in naturally fed animals was related to the presence of anti-BSA antibodies in breast milk and/or in plasma of the pups, breast milk and plasma from the breast-fed animals was evaluated by counterimmunoelectrophoresis and hemagglutination. No anti-BSA antibodies were detected. Moreover, plasma from breast- and artificially fed rabbits not gavage fed BSA contained no I-BSA. These data suggest that intestinal transport of antigens in the immediate neonatal period is decreased earlier in breast- as compared to bottle-fed animals. Therefore, we suggest that breast milk may exert a protective function to control the transport of potentially antigenic molecules into the systemic circulation of newborn animals by either facilitating the early maturation of intestinal barrier function or by providing passive barrier factors until the newborn's natural barrier can develop.

Animal Feed↗
PubMed2006

Chronic acid water feeding protects mice against lethal gut-derived sepsis due to Pseudomonas aeruginosa.

Acidified feeding formulas have been proposed as a method of controlling gastrointestinal colonization and nosocomial infection in critically ill patients. We examined possible mechanisms by which chronic acid water feeding might protect the host against lethal gut derived sepsis by assessing its effect on both local intestinal epithelial barrier function to bacteria as well as on local and systemic heat shock protein expression. Heat shock protein expression measured by immunoblot demonstrated that HSP25 was increased in the stomach, aorta and kidney of mice chronically fed acid water (8 weeks) compared to tap water fed controls. HSP72 expression was also increased in the aorta of mice drinking acid water. The protein content of cecum and its barrier function were enhanced in mice ingesting acidified water. The direct effect of an acid environment on intestinal epithelial barrier function was tested in cultured human intestinal epithelial cells. An acidified environment protected against bacterial mediated disruption of the intestinal epithelial barrier. Finally, the protective effect of chronic acid water feeding on gut-derived sepsis due to P. aeruginosa was tested in mice. Chronic acid water feeding protected mice from the lethal gut derived sepsis due to P. aeruginosa.

Animals↗
PubMed1997

Review article: Intestinal epithelia and barrier functions.

The mucosal epithelia of the digestive tract acts as a selective barrier, permeable to ions, small molecules and macromolecules. These epithelial cells aid the digestion of food and absorption of nutrients. They contribute to the protection against pathogens and undergo continuous cell renewal which facilitates the elimination of damaged cells. Both innate and adaptive defence mechanisms protect the gastrointestinal-mucosal surfaces against pathogens. Interaction of microorganisms with epithelial cells triggers a host response by activating specific transcription factors which control the expression of chemokines and cytokines. This host response is characterized by the recruitment of macrophages and neutrophils at the site of infection. Disruption of epithelial signalling pathways that recruit migratory immune cells results in a chronic inflammatory response. The adaptive defence mechanism relies on the collaboration of epithelial cells (resident sampling system) with antigen-presenting and lymphoid cells (migratory sampling system); in order to obtain samples of foreign antigen, these samples must be transported across the barriers without affecting the integrity of the barrier. These sampling systems are regulated by both environmental and host factors. Fates of the antigen may differ depending on the way in which they cross the epithelial barrier, i.e. via interaction with motile dendritic cells or epithelial M cells in the follicle-associated epithelium.

Adaptation, Physiological↗
PubMed2003

Regulation of adherens junctions and epithelial paracellular permeability: a novel function for polyamines.

Maintenance of intestinal mucosal epithelial integrity requires polyamines that are involved in the multiple signaling pathways controlling gene expression and different epithelial cell functions. Integrity of the intestinal epithelial barrier depends on a complex of proteins composing different intercellular junctions, including tight junctions, adherens junctions, and desmosomes. E-cadherin is primarily found at the adherens junctions and plays a critical role in cell-cell adhesions that are fundamental to formation of the intestinal epithelial barrier. The current study determined whether polyamines regulate intestinal epithelial barrier function by altering E-cadherin expression. Depletion of cellular polyamines by alpha-difluoromethylornithine (DFMO) reduced intracellular free Ca2+ concentration ([Ca2+]cyt), decreased E-cadherin expression, and increased paracellular permeability in normal intestinal epithelial cells (IEC-6 line). Polyamine depletion did not alter expression of tight junction proteins such as zona occludens (ZO)-1, ZO-2, and junctional adhesion molecule (JAM)-1. Addition of exogenous polyamine spermidine reversed the effects of DFMO on [Ca2+]cyt and E-cadherin expression and restored paracellular permeability to near normal. Elevation of [Ca2+]cyt by the Ca2+ ionophore ionomycin increased E-cadherin expression in polyamine-deficient cells. In contrast, reduction of [Ca2+]cyt by polyamine depletion or removal of extracellular Ca2+ not only inhibited expression of E-cadherin mRNA but also decreased the half-life of E-cadherin protein. These results indicate that polyamines regulate intestinal epithelial paracellular barrier function by altering E-cadherin expression and that polyamines are essential for E-cadherin expression at least partially through [Ca2+]cyt.

Adherens Junctions↗
PubMed1997

Changes in barrier function of a model intestinal epithelium by intraepithelial lymphocytes require new protein synthesis by epithelial cells.

BACKGROUND: Elements of the mucosal immune system may play an important part in regulating epithelial barrier function in the intestinal tract. Intraepithelial lymphocytes (IELs) represent a subtype of immunocyte which is strategically placed to regulate epithelial function at most mucosal sites. AIMS AND METHODS: An IEL derived cell line (SC1) was used to examine its effects on the model epithelium T84--a tumour derived cell line which retains the phenotype of colonic crypt cells. Transepithelial electrical resistance (TER) was used as a marker of epithelial integrity. RESULTS: Coculture of T84 cells with SC1 produced a significant fall in TER as did exposure of T84 monolayers to IEL derived supernatant. Recombinant interferon-gamma (rIFN gamma) also reduced TER in T84 monolayers. Cycloheximide prevented the effects of IEL supernatant and of rIFN gamma on TER. The fall in TER in response to rIFN gamma was attenuated by blocking antibodies, which did not alter the fall in resistance induced by IEL supernatant. Fractions of IEL supernatant, separated on the basis of size, evoked temporally distinct changes in TER. Ultrastructural studies support the hypothesis that the slow onset but severe fall in TER indicates catastrophic effects on the monolayer. The more rapid onset fall in TER was not associated with gross changes in monolayer morphology. Reduction of TER by IEL supernatant was not influenced by inhibitors of tyrosine phosphatase or of protein kinase C. Although herbimycin did reduce the rapid onset change in TER, the tyrosine kinase inhibitor genistein did not alter responses to IEL supernatant. CONCLUSIONS: Mucosal T cells may influence barrier function by a process involving new protein synthesis by epithelial cells. This model may have relevance in some inflammatory conditions of the gastrointestinal tract.

Benzoquinones↗
PubMed2002

Intestinal infection with Giardia spp. reduces epithelial barrier function in a myosin light chain kinase-dependent fashion.

BACKGROUND & AIMS: Giardiasis causes malabsorptive diarrhea, and symptoms can be present in the absence of any significant morphologic injury to the intestinal mucosa. The effects of giardiasis on epithelial permeability in vivo remain unknown, and the role of T cells and myosin light chain kinase (MLCK) in altered intestinal barrier function is unclear. This study was conducted to determine whether Giardia spp. alters intestinal permeability in vivo, to assess whether these abnormalities are dependent on T cells, and to assess the role of MLCK in altered epithelial barrier function. METHODS: Immunocompetent and isogenic athymic mice were inoculated with axenic Giardia muris trophozoites or sterile vehicle (control), then assessed for trophozoite colonization and gastrointestinal permeability. Mechanistic studies using nontransformed human duodenal epithelial monolayers (SCBN) determined the effects of Giardia on myosin light chain (MLC) phosphorylation, transepithelial fluorescein isothiocyanate-dextran fluxes, cytoskeletal F-actin, tight junctional zonula occludens-1 (ZO-1), and MLCK. RESULTS: Giardia infection caused a significant increase in small intestinal, but not gastric or colonic, permeability that correlated with trophozoite colonization in both immunocompetent and athymic mice. In vitro, Giardia increased permeability and phosphorylation of MLC and reorganized F-actin and ZO-1. These alterations were abolished with an MLCK inhibitor. CONCLUSIONS: Disruption of small intestinal barrier function is T cell independent, disappears on parasite clearance, and correlates with reorganization of cytoskeletal F-actin and tight junctional ZO-1 in an MLCK-dependent fashion.

Actins↗
PubMed2003

Alterations of intestinal mucosa structure and barrier function following traumatic brain injury in rats.

AIM: Gastrointestinal dysfunction is a common complication in patients with traumatic brain injury (TBI). However, the effect of traumatic brain injury on intestinal mucosa has not been studied previously. The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly the impairment of gut barrier function occurs and how long it persists following traumatic brain injury. METHODS: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, and 72, and on day 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability was measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. RESULTS: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, damage of mitochondria and endoplasm, were found by electron microscopy. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. As compared with that of control group (183.7 +/- 41.8 EU/L), serum endotoxin level was significantly increased at 3, 12, and 24 hours following TBI (434.8 +/- 54.9 EU/L, 324.2 +/- 61.7 EU/L and 303.3 +/- 60.2 EU/L, respectively), and peaked at 72 hours (560.5 +/- 76.2 EU/L), then declined on day 7 (306.7 +/- 62.4 EU/L, P<0.01). Two peaks of serum endotoxin level were found at hours 3 and 72 following TBI. L/M ratio was also significantly higher in TBI groups than that in control group (control, 0.0172 +/- 0.0009; 12 h, 0.0303 +/- 0.0013; 24 h, 0.0354 +/- 0.0025; 72 h, 0.0736 +/- 0.0105; 7 d, 0.0588 +/- 0.0083; P<0.01). CONCLUSION: Traumatic brain injury can induce significant damages of gut structure and impairment of barrier function which occur rapidly as early as 3 hours following brain injury and lasts for more than 7 days with marked mucosal atrophy.

Animals↗
PubMed1985

Macromolecular transport in the fetal rat intestine.

Macromolecular barrier function of the fetal rat small intestine and colon was analyzed from 16 to 22 days gestation (birth). During this period the epithelium is converted from stratified to simple columnar. To assess permeability, horseradish peroxidase (HRP) was introduced by microinjection into the lumen or into the umbilical circulation. Proximal small intestine, distal small intestine, and colon were examined after 10-20 min. Paracellular passage of HRP through occluding junctions was not observed after either intraluminal or intravascular injection. After intraluminal injection, transepithelial transport of HRP from lumen to blood occurred in all regions at all ages studied. Horseradish peroxidase was present in cytoplasmic vesicles of most cells in the primitive stratified epithelia, during epithelial conversion, and in simple columnar epithelia. After intravascular injection, HRP was present in the lamina propria and in intercellular spaces of the epithelium, but HRP did not enter tight junctions. Tracer was taken up into cytoplasmic vesicles of both stratified and simple columnar epithelial cells, but was only rarely seen in the lumen. We conclude that there is rapid transcellular, vesicle-mediated transport from lumen to blood across both stratified and simple columnar epithelia of fetal rat small intestine and colon; after intravascular injection, macromolecules may be taken up into vesicles at basolateral epithelial cell surfaces but are not rapidly transported into the lumen; paracellular passage does not occur in the fetal ages studied.

Animals↗
PubMed1998

Impedance analysis for the determination of epithelial and subepithelial resistance in intestinal tissues.

The barrier function of the intestinal wall plays a key role in body homeostasis and defense against noxious agents. Conventional Ussing chamber techniques determine the overall transmural resistance but do not differentiate epithelial and subepithelial tissues. The barrier function, however, resides in the epithelial cell layer only. Transmural impedance analysis can solve this problem, if adequate models are applied. We show that: (i) epithelial and subepithelial impedances are additive, (ii) the epithelium proper can be represented by a very general electrical model, which demonstrates short-circuiting at high frequencies (due to cell membrane capacitances), and (iii) the reactance of subepithelial tissue can be described phenomenologically. Using an empirical expression for description of the subepithelial impedance, the present method allows the determination of the epithelial and the subepithelial resistance. This was exemplified in rat ileum, which defied adequate impedance analysis so far. Of the transmural DC resistance of 61 +/- 5 omega.cm2 (n = 8) the subepithelial contribution was 28 +/- 2 omega.cm2 and the epithelial resistance was 33 +/- 4 omega.cm2.

Animals↗
PubMed2002

A membrane-permeant peptide that inhibits MLC kinase restores barrier function in in vitro models of intestinal disease.

BACKGROUND & AIMS: Maintenance of the mucosal barrier is a critical function of intestinal epithelia. Myosin regulatory light chain (MLC) phosphorylation is a common intermediate in the pathophysiologic regulation of this barrier. The aim of this study was to determine whether a membrane permeant inhibitor of MLC kinase (PIK) could inhibit intracellular MLC kinase and regulate paracellular permeability. METHODS: Recombinant MLC and Caco-2 MLC kinase were used for kinase assays. T84 and Caco-2 monolayers were treated with enteropathogenic Escherichia coli (EPEC) or tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma to induce barrier dysfunction. RESULTS: PIK inhibited MLC kinase in vitro and was able to cross cell membranes and concentrate at the perijunctional actomyosin ring. Consistent with these properties, apical addition of PIK reduced intracellular MLC phosphorylation by 22% +/- 2%, increased transepithelial resistance (TER) by 50% +/- 1%, and decreased paracellular mannitol flux rates by 5.2 +/- 0.2-fold. EPEC infection induced TER decreases of 37% +/- 6% that were limited to 16% +/- 5% by PIK. TNF-alpha and IFN-gamma induced TER decreases of 22% +/- 3% that were associated with a 172% +/- 1% increase in MLC phosphorylation. Subsequent PIK addition caused MLC phosphorylation to decrease by 25% +/- 4% while TER increased to 97% +/- 6% of control. CONCLUSIONS: PIK can prevent TER defects induced by EPEC and reverse MLC phosphorylation increases and TER decreases induced by TNF-alpha and IFN-gamma. The data also suggest that TNF-alpha and IFN-gamma regulate TER, at least in part, via the perijunctional cytoskeleton. Thus, PIK may be the prototype for a new class of targeted therapeutic agents that can restore barrier function in intestinal disease states.

Actomyosin↗
PubMed2006

Role of intestinal barrier in pathogenesis of pigment gallstone in a guinea pig model.

BACKGROUND: The function of the intestinal barrier has drawn more and more attention from researchers in recent years for its important role in many diseases such as burns, wounds, and pancreatitis. In our experimental studies on pigment gallstone, we found potential relationships between the function of the intestinal barrier and pigment gallstone formation. This study was undertaken to investigate the possible action and mechanism of the function of the intestinal barrier in the pathogenesis of pigment gallstone. METHODS: Eighty guinea pigs were divided into a normal group (CON), a pigment gallstone group (PS) and an intestinal mucosa protection group (GLN). Normal forage, pigment gallstone-forming forage and pigment gallstone-forming forage with supplemental intestinal mucosa protector (glutamine) were given to each group. In the gallstone-forming rate, morphology of intestinal mucosa, intestinal permeability, serum endotoxin and biliary beta-glucuronidase were assessed after 8 weeks. RESULTS: The rate of gallstone-formation was 73.9% in the PS group. Damage of intestinal mucosa, endotoxemia (from 77+/-43 X 10(-6) EU/L to 1,367+/-525 X 10(-6) EU/L, P<0.01) and increased activity of biliary beta-glucuronidase (endogenous beta-glucuronidase from 122.1+/-39.5 to 209.8+/-47.5 Fishman Unit, P<0.01, and exogenous beta-glucuronidase from 573.5+/-476.9 to 2,206.6+/-983.9 Fishman Unit, P<0.01) were observed in the PS group compared with the CON group. The rate gallstone-formation decreased significantly to 44.4% and the other indices except beta-glucuronidase were lower in the GLN group than in the PS group. CONCLUSIONS: The function of the intestinal barrier is correlated with pigment gallstone formation. Dysfunction of the intestinal barrier function may promote pigment gallstone formation through bacterial translocation, endotoxemia, and biliary beta-glucuronidase.

Animals↗
PubMed1996

Intestinal barrier dysfunction in clinical and experimental obstructive jaundice and its reversal by internal biliary drainage.

Intestinal mucosal barrier function in obstructive jaundice was assessed in an animal model and in patients. The effect of internal biliary drainage in patients was also examined. Bile duct ligation for 1 week in the rat resulted in significant bacterial translocation (in seven of 12 animals following ligation versus none of the shamoperated controls, P < 0.01). Intestinal permeability, measured by the urinary recovery of orally administered polyethylene glycol, was also significantly increased (+66.2 per cent for ligation versus -11.6 per cent for sham, P < 0.01). A prospective study was performed on 33 patients with obstructive jaundice undergoing internal biliary drainage, and results were compared with those in six non-jaundiced patients undergoing laparotomy or endoscopic retrograde cholangiopancreatography and in 11 health volunteers. The lactulose: mannitol ratio was used as an intestinal permeability index. Mean(s.e.m.) intestinal permeability assessed before operation was significantly increased in jaundiced patients compared with control patients (0.050(0.010) versus 0.016(0.003), P < 0.005). The mean(s.e.m.) lactulose: mannitol ratio in the healthy volunteers was 0.020(0.003), which was similar to that in control patients. In the jaundiced group of patients the intestinal permeability index fell to within normal levels after 28 days of internal biliary drainage (0.050 before operation versus 0.021 at 28 days, P < 0.02). These data indicate that intestinal barrier function is impaired in obstructive jaundice and that this impairment is reversed by return of bile to the gastrointestinal tract.

Animals↗
PubMed1997

Epithelial cell kinase-B61: an autocrine loop modulating intestinal epithelial migration and barrier function.

Epithelial cell kinase (Eck) is a member of a large family of receptor tyrosine kinases whose functions remain largely unknown. Expression and regulation of Eck and its cognate ligand B61 were analyzed in the human colonic adenocarcinoma cell line Caco-2. Immunocytochemical staining demonstrated coexpression of Eck and B61 in the same cells, suggestive of an autocrine loop. Eck levels were maximal in preconfluent cells. In contrast, B61 levels were barely detectable in preconfluent cells and increased progressively after the cells reached confluence. Caco-2 cells cultured in the presence of added B61 showed a significant reduction in the levels of dipeptidyl peptidase and sucrase-isomaltase mRNA, markers of Caco-2 cell differentiation. Cytokines interleukin-1beta (IL-1beta), basic fibroblast growth factor, IL-2, epidermal growth factor, and transforming growth factor-beta modulated steady-state levels of Eck and B61 mRNA and regulated Eck activation as assessed by tyrosine phosphorylation. Functionally, stimulation of Eck by B61 resulted in increased proliferation, enhanced barrier function, and enhanced restitution of injured epithelial monolayers. These results suggest that the Eck-B61 interaction, a target of regulatory peptides, plays a role in intestinal epithelial cell development, migration, and barrier function, contributing to homeostasis and preservation of continuity of the epithelial barrier.

Adenocarcinoma↗
PubMed2002

Delayed consequences of protein deficiency during lactation for the development of enzyme systems of digestive and nondigestive organs in offspring.

Suboptimal protein nutrition during lactation has a negative impact on the digestive function of the small intestine and trophic barrier functions of the large intestine, liver, and kidneys due to significant enzyme deficiency (disaccharidase, peptidase, alkaline phosphatase) in 6-month-old offspring. Changes in enzyme activity in digestive and nondigestive organs play an important role in metabolic disorders promoting the development of "risk diseases" and reducing lifespan.

Animals↗
PubMed2002

Intestinal permeability and carrier-mediated monosaccharide absorption in preterm neonates during the early postnatal period.

Immaturity of intestinal epithelial barrier function and absorptive capacity may play a role in the pathophysiology of intestinal complications in preterm neonates during the early postnatal period. We determined the intestinal permeability and carrier-mediated absorption of monosaccharides in preterm neonates during the first 2 wk after birth. Fifty-nine preterm neonates born between 25 and 32 wk gestation were included within 24 h of birth. Neonates received exclusively parenteral nutrition during the first 7 d after birth; enteral feeding was initiated at d 8. An intestinal permeability-absorption test was performed at 1, 4, 7, and 14 d after birth. The lactulose-to-rhamnose ratio was determined as a marker of intestinal permeability. Urinary excretion percentages of D-xylose and 3-O-methyl-D-glucose were determined as markers of passive and active carrier-mediated monosaccharide absorption, respectively. Intestinal permeability transiently increased between d 1 and 7 in all neonates (p < 0.05). Carrier-mediated monosaccharide absorption increased between d 1 and 14 in neonates of 28-30 wk (p < 0.05) to the level observed in the neonates of 30-32 wk gestation. In neonates <28 wk, intestinal permeability at d 7 was higher (p < 0.05) and carrier-mediated monosaccharide absorption at d 14 was lower (p < 0.01) as compared with neonates >or=28 wk. The barrier function of the intestinal epithelium transiently decreases during the first week after birth in preterm neonates who are not enterally fed. Diminished barrier function and low monosaccharide absorptive capacity, particularly in neonates <28 wk, may predispose these patients to the development of intestinal complications during the early postnatal period.

Female↗
PubMed2005

Effect of acute alcohol ingestion prior to burn injury on intestinal bacterial growth and barrier function.

Previous studies from our laboratory have shown that acute alcohol (EtOH) ingestion prior to burn injury enhances intestinal bacterial translocation. This study tested if increased intestinal bacterial translocation in alcohol and burn injured rats is due to an overgrowth in intestinal bacteria. We determined if the translocation was accompanied with alterations in intestinal permeability and immune cell population. Rats (225-250 g) were gavaged with alcohol to achieve a blood EtOH level in the range of 100 mg/dl prior to burn or sham injury (25% total body surface area). Two days after injury, we found that acute alcohol ingestions prior to burn injury results in a significant increase in bacterial counts in small intestine. The increase in intestinal bacterial counts accompanied a significant increase in intestinal permeability. Finally, immunohistochemical analysis revealed a substantial (p<0.05) loss of both T cell and dendritic cells in intestine of alcohol and burn injured rats compared with intestine of rats receiving either burn or sham injury. Altogether, results presented in this manuscript suggest that increase in intestinal bacterial growth along with alterations in intestinal permeability and immune status contribute to the increase in bacterial translocation observed in alcohol and burn injured rats.

Animals↗