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PubMed2001

Stress and gastrointestinal tract. II. Stress and intestinal barrier function.

The influence of stress on the clinical course of a number of intestinal diseases is increasingly being recognized, but the underlying mechanisms are largely unknown. This themes article focuses on recent findings related to the effects of stress on mucosal barrier function in the small intestine and colon. Experiments using animal models demonstrate that various types of psychological and physical stress induce dysfunction of the intestinal barrier, resulting in enhanced uptake of potentially noxious material (e.g., antigens, toxins, and other proinflammatory molecules) from the gut lumen. Evidence from several studies indicates that in this process, mucosal mast cells play an important role, possibly activated via neurons releasing corticotropin-releasing hormone and/or acetylcholine. Defining the role of specific cells and mediator molecules in stress-induced barrier dysfunction may provide clues to novel treatments for intestinal disorders.

Animals↗
PubMed2001

Key role of PKC and Ca2+ in EGF protection of microtubules and intestinal barrier against oxidants.

Using monolayers of human intestinal (Caco-2) cells, we showed that growth factors (GFs) protect microtubules and barrier integrity against oxidative injury. Studies in nongastrointestinal cell models suggest that protein kinase C (PKC) signaling is key in GF-induced effects and that cytosolic calcium concentration ([Ca2+](i)) is essential in cell integrity. We hypothesized that GF protection involves activating PKC and maintaining normal ([Ca2+](i)) Monolayers were pretreated with epidermal growth factor (EGF) or PKC or Ca2+ modulators before exposure to oxidants (H2O2 or HOCl). Oxidants disrupted microtubules and barrier integrity, and EGF protected from this damage. EGF caused rapid distribution of PKC-alpha, PKC-betaI, and PKC-zeta isoforms to cell membranes, enhancing PKC activity of membrane fractions while reducing PKC activity of cytosolic fractions. EGF enhanced (45)Ca2+ efflux and prevented oxidant-induced (sustained) rises in ([Ca2+](i)). PKC inhibitors abolished and PKC activators mimicked EGF protection. Oxidant damage was mimicked by and potentiated by a Ca2+ ionophore (A-23187), exacerbated by high-Ca2+ media, and prevented by calcium removal or chelation or by Ca2+ channel antagonists. PKC activators mimicked EGF on both (45)Ca2+ efflux and ([Ca2+](i)). Membrane Ca2+-ATPase pump inhibitors prevented protection by EGF or PKC activators. In conclusion, EGF protection of microtubules and the intestinal epithelial barrier requires activation of PKC signal transduction and normalization of ([Ca2+](i)).

Calcimycin↗
PubMed2005

Differential transfer of organic micropollutants through intestinal barrier using Caco-2 cell line.

Food seems to be one of the main ways of animal and human contamination with polycyclic aromatic hydrocarbons (PAHs) and dioxins. In vivo studies showed a blood absorption of these xenobiotics after their ingestion. Our work aimed at studying the in vitro transfer of PAHs and dioxins through intestinal barrier. Caco-2 cells were cultivated on permeable filters to measure transepithelial permeability of (14)C labeled 2,3,7,8-tetrachlorodibenzo-p-dioxin, benzo[a]pyrene, pyrene, and phenanthrene, which differed in their physicochemical properties. The results showed that the molecules were able to cross intestinal cell layers. All the molecules were detected associated with cells, even if the dioxin was the less uptaken compound. Phenanthrene appeared in basal media faster, and its level after a 6-h exposure was respectively 1.1, 2, and 7 times higher than pyrene, benzo[a]pyrene, and 2,3,7,8-tetrachlorodibenzo-p-dioxin levels. These findings suggest that intestinal epithelium plays a key role in selective permeability and then in bioavailibility of micropollutants.

Biological Transport↗
PubMed2001

Translocated EspF protein from enteropathogenic Escherichia coli disrupts host intestinal barrier function.

The mechanisms by which enteropathogenic Escherichia coli (EPEC), an important cause of diarrhea among infants in developing countries, induce symptoms are not defined. EPEC have a type III secretion system required for characteristic attaching and effacing changes that modify the cytoskeleton and apical surface of host cells. Infection of polarized intestinal epithelial cell monolayers by EPEC leads to a loss of transepithelial electrical resistance, which also requires the type III secretion system. We demonstrate here that EspF, a protein that is secreted by EPEC via the type III secretion system, is not required for quantitatively and qualitatively typical attaching and effacing lesion formation in intestinal epithelial cells. However, EspF is required in a dose-dependent fashion for the loss of transepithelial electrical resistance, for increased monolayer permeability, and for redistribution of the tight junction-associated protein occludin. Furthermore, the analysis of EPEC strains expressing EspF-adenylate cyclase fusion proteins indicates that EspF is translocated via the type III secretion system to the cytoplasm of host cells, a result confirmed by immunofluorescence microscopy. These studies suggest a novel role for EspF as an effector protein that disrupts intestinal barrier function without involvement in attaching and effacing lesion formation.

Bacterial Adhesion↗
PubMed1999

[Acute failure of the intestinal barrier--pathophysiology, diagnosis, prophylaxis and therapy].

The gut not only serves as a main target for the detrimental effects of stress during and after surgery, but may also promote the development of multiple organ failure after different types of severe shock. According to a current hypothesis, an impaired intestinal barrier function is associated with a decreased separation of intraluminal bacteria and toxins and systemic circulation, which may induce sepsis and multiple organ failure. Hypoperfusion during shock, reperfusion injury of the splanchnic mucosa, alterations of the micro-ecology of the gut and immunologic and hormonal disturbances are important underlying pathophysiological mechanisms. Various therapeutic concepts have been proposed such as improvement of splanchnic perfusion, nutritive and metabolic treatment by means of immunomodulating nutrients, parenteral substitution of glutamine, early onset of enteral nutrition, normalization of gut motility and selective decontamination of the gut. However, no clinical study to date could clearly demonstrate a key role of the gut in the pathogenesis of sepsis and multiple organ failure. Likewise, the efficacy of different prophylactic and therapeutic procedures remain to be studied. An aggressive treatment of shock and avoidance of microcirculatory disturbances are of principal importance for prophylaxis of multiple organ failure.

Acute Disease↗
PubMed2002

HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice.

BACKGROUND & AIMS: High mobility group (HMG) B1 is a nonhistone nuclear protein that was recently identified as a late-acting mediator of lipopolysaccharide-induced lethality in mice. The proinflammatory actions of HMGB1 have been localized to a region of the molecule called the B box. METHODS: To determine whether HMGB1 or B box are capable of causing derangements in intestinal barrier function, we incubated cultured Caco-2 human enterocytic monolayers with recombinant human HMGB1 or a 74-residue truncated form of the protein consisting of the B box domain. RESULTS: Both HMGB1 and B box increased the permeability of Caco-2 monolayers to fluorescein isothiocyanate-labeled dextran (FD4) in a time- and dose-dependent fashion. The increase in permeability was reversible following removal of the recombinant protein. Exposure of Caco-2 cells to B box resulted in increased expression of inducible nitric oxide synthase messenger RNA and increased production of NO. When we used various pharmacologic strategies to inhibit NO production or scavenge NO or peroxynitrite (ONOO(-)), we abrogated B box-induced hyperpermeability. Administration of B box to wild-type mice increased both ileal mucosal permeability to FD4 and bacterial translocation to mesenteric lymph nodes. These effects were not observed in inducible nitric oxide synthase knockout mice. CONCLUSIONS: These data support the view that HMGB1 and B box are capable of causing alterations in gut barrier function via a mechanism that depends on the formation of NO and ONOO(-).

Animals↗
PubMed2006

Probiotics prevent bacterial translocation and improve intestinal barrier function in rats following chronic psychological stress.

BACKGROUND AND AIMS: Chronic psychological stress, including water avoidance stress (WAS), induces intestinal mucosal barrier dysfunction and impairs mucosal defences against luminal bacteria. The aim of this study was to determine the ability of a defined probiotic regimen to prevent WAS induced intestinal pathophysiology. METHODS: Male rats were subjected to either WAS or sham stress for one hour per day for 10 consecutive days. Additional animals received seven days of Lactobacillus helveticus and L rhamnosus in the drinking water prior to stress and remained on these probiotics for the duration of the study. Rats were then sacrificed, intestinal segments assessed in Ussing chambers, and mesenteric lymph nodes cultured to determine bacterial translocation. RESULTS: All animals remained healthy for the duration of the study. Chronic WAS induced excess ion secretion (elevated baseline short circuit current) and barrier dysfunction (increased conductance) in both the ileum and colon, associated with increased bacterial adhesion and penetration into surface epithelial cells. Approximately 70% of rats subjected to WAS had bacterial translocation to mesenteric lymph nodes while there was no bacterial translocation in controls. Probiotic pretreatment alone had no effect on intestinal barrier function. However, WAS induced increased ileal short circuit current was reduced with probiotics whereas there was no impact on altered conductance. Pretreatment of animals with probiotics also completely abrogated WAS induced bacterial adhesion and prevented translocation of bacteria to mesenteric lymph nodes. CONCLUSION: These findings indicate that probiotics can prevent chronic stress induced intestinal abnormalities and, thereby, exert beneficial effects in the intestinal tract.

Animals↗
PubMed2005

The role of protein kinase C isoforms in modulating injury and repair of the intestinal barrier.

Gastrointestinal cells express a diverse group of protein kinase C (PKC) isoforms that play critical roles in a number of cell functions, including intracellular signaling and barrier integrity. PKC isoforms expressed by gastrointestinal epithelial cells consist of three major PKC subfamilies: conventional isoforms (alpha, beta1, beta2, and gamma), novel isoforms (delta, epsilon, theta, eta, and mu), and atypical isoforms (lambda, tau, and zeta). This review highlights recent discoveries, including our own, that some PKC isoforms in gastrointestinal epithelia monolayer cell culture are involved in injury to, whereas others are involved in protection of, intestinal barrier integrity. For example, certain PKC isoforms aggravate oxidative damage, whereas others protect against it. These findings suggest that the development of agents that selectively activate or inhibit specific PKC isoforms may lead to new therapeutic modalities for important gastrointestinal disorders such as cancer and inflammatory bowel disease.

Animals↗
PubMed2005

Bifidobacterium breve and Streptococcus thermophilus secretion products enhance T helper 1 immune response and intestinal barrier in mice.

Lactic acid bacteria or their secretion products can modulate immune responses differently in normal and inflammatory conditions. This comparative study analyzes the effect of oral administration of living lactic acid bacteria, or their conditioned media, on the epithelial and immune functions of colitis-prone C57BL/6 IL-10-deficient mice. Mice were untreated (control) or infected with Helicobacter hepaticus with or without oral treatment with living bacteria, Bifidobacterium breve C50 and Streptococcus thermophilus 065 (LB), or their culture-conditioned media (CM). Histology, cytokine mRNA, electrical resistance, and barrier capacity of colonic samples as well as cytokine secretion by mesenteric lymph node (MLN) cells were studied. Helicobacter hepaticus mice developed only mild colitis, which was not modified in LB or CM groups. In the CM (but not the LB) group, the colonic barrier was reinforced as compared to the other groups, as evidenced by decreased horseradish peroxidase (HRP) transcytosis and mannitol fluxes and increased electrical resistance. In MLN, the percentage of CD4+ and CD8+ T cells secreting IFNgamma was significantly higher in CM (2.06% and 1.98%, respectively) mice than in H. hepaticus (1.1% and 0.47%, P < 0.05) or control mice. In addition, the nonspecific stimulation of IFNgamma, TNFalpha, and IL-12 secretion by MLN cells was significantly higher in the CM group as compared to the other groups. In the absence of severe colitis, Bifidobacterium breve C50- and Streptococcus thermophilus 065-conditioned media can reinforce intestinal barrier capacity and stimulate Th1 immune response, highlighting the involvement of lactic acid bacteria-derived components in host defense.

Animals↗
PubMed2001

Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia.

This work tested the hypotheses that splanchnic oxidant generation is important in determining heat tolerance and that inappropriate.NO production may be involved in circulatory dysfunction with heat stroke. We monitored colonic temperature (T(c)), heart rate, mean arterial pressure, and splanchnic blood flow (SBF) in anesthetized rats exposed to 40 degrees C ambient temperature. Heating rate, heating time, and thermal load determined heat tolerance. Portal blood was regularly collected for determination of radical and endotoxin content. Elevating T(c) from 37 to 41.5 degrees C reduced SBF by 40% and stimulated production of the radicals ceruloplasmin, semiquinone, and penta-coordinate iron(II) nitrosyl-heme (heme-.NO). Portal endotoxin concentration rose from 28 to 59 pg/ml (P < 0.05). Compared with heat stress alone, heat plus treatment with the nitric oxide synthase (NOS) antagonist N(omega)-nitro-L-arginine methyl ester (L-NAME) dose dependently depressed heme-.NO production and increased ceruloplasmin and semiquinone levels. L-NAME also significantly reduced lowered SBF, increased portal endotoxin concentration, and reduced heat tolerance (P < 0.05). The NOS II and diamine oxidase antagonist aminoguanidine, the superoxide anion scavenger superoxide dismutase, and the xanthine oxidase antagonist allopurinol slowed the rates of heme-.NO production, decreased ceruloplasmin and semiquinone levels, and preserved SBF. However, only aminoguanidine and allopurinol improved heat tolerance, and only allpourinol eliminated the rise in portal endotoxin content. We conclude that hyperthermia stimulates xanthine oxidase production of reactive oxygen species that activate metals and limit heat tolerance by promoting circulatory and intestinal barrier dysfunction. In addition, intact NOS activity is required for normal stress tolerance, whereas overproduction of.NO may contribute to the nonprogrammed splanchnic dilation that precedes vascular collapse with heat stroke.

Allopurinol↗
PubMed2005

The role of enterocytes in the intestinal barrier function and antigen uptake.

The intestinal epithelium is a critical interface between the organism and its environment. The cell polarity and structural properties of the enterocytes, limiting the amount of antigen reaching the epithelial surface, form the basis of the integrity of the epithelium. However, apart from their participation in digestive processes, the enterocytes perform more than just a passive barrier function. The resistance of the tight junctions regulates the paracellular transport of antigens. Furthermore, the enterocytes take up and process antigens, involving two functional pathways. In the major pathway, enzymes in the lysosomes degrade the antigens. In the minor direct transcytotic pathway, the antigens are not degraded and are released into the interstitial space. Moreover, the enterocytes can present processed antigens directly to T cells and are often directly involved in immune processes. In inflammatory conditions, the properties of the epithelial barrier and the outcome of the immune response to luminal antigens can be changed.

Animals↗
PubMed1998

The effect of tacrolimus (FK506) on intestinal barrier function and cellular energy production in humans.

BACKGROUND & AIMS: The maintenance of the intestinal mucosal barrier may be energy dependent. Tacrolimus is a potent immunosuppressive drug that decreases mitochondrial adenosine triphosphate production and increases intestinal permeability in animals. METHODS: Twelve liver graft recipients receiving tacrolimus, 9 healthy volunteers, and 5 liver graft recipients not receiving immunosuppression underwent a combined absorption-permeability-mitochondrial function test using 5 g lactulose, 1 g L-rhamnose, 0.5 g D-xylose, 0.2 g 3-O-methyl-D-glucose, 1 mg/kg 2-keto[1-13C]isocaproic acid ([13C]KICA), and 20 mg/kg L-leucine. The respiratory quotient and resting energy expenditure were measured by indirect calorimetry. Tacrolimus pharmacokinetic profiles and levels of endotoxin and IgM and IgG endotoxin core antibodies were determined. RESULTS: Tacrolimus inhibited the decarboxylation of [13C]KICA, the resting energy expenditure, and the respiratory quotient in an exposure-dependent manner, suggesting an inhibition of mitochondrial respiration. Tacrolimus inhibited intestinal absorptive capacity in an exposure-dependent manner. Tacrolimus-treated patients had an increased intestinal permeability and significantly higher endotoxin levels compared with healthy volunteers. CONCLUSIONS: Tacrolimus inhibits cellular energy production in humans at clinically relevant doses. This is associated with an increased intestinal permeability, endotoxemia, and an impaired intestinal absorptive capacity.

Adolescent↗
PubMed2004

Mechanisms of postburn intestinal barrier dysfunction in the rat: roles of epithelial cell renewal, E-cadherin, and neutrophil extravasation.

OBJECTIVE: Our group has previously shown that the intestinal epithelium exhibits increased postburn barrier permeability and bacterial translocation associated with deranged neutrophil activity. The purpose of this investigation is to explore possible underlying intestinal structural mechanisms, leading to those functional changes with emphasis on (1) neutrophil influx and extravasation in the intestinal lamina propria 1-3 days after burn and (2) enterocyte proliferation, migration, apoptosis, and E-cadherin junctional epithelium levels 3 days after burn. DESIGN: Freshly isolated ileum specimens were quick frozen, then cut by a cryostat into 30-micron-thick sections. Sections from day 1 postburn rats were immunostained with (1) anti-granulocyte or anti-elastase antibodies to assess neutrophil influx or (2) combined anti-granulocyte and anti-von Willebrand factor double immunolabeling to compare levels of neutrophil extravasation. Sections from day 3 postburn rats were immunostained with (1) bromodeoxyuridine immunohistochemistry 1, 3, 6, or 18 hrs after bromodeoxyuridine injection to assess enterocyte proliferation and migration, (2) cytokeratin-18 M30-immunohistochemistry to compare levels of enterocyte apoptosis, and (3) E-cadherin immunohistochemistry to compare junctional E-cadherin integrity. Ileal myeloperoxidase activity and bacterial translocation of Enterococcus faecalis were assessed biochemically and by E. faecalis-specific bacterial cultures, respectively, in day 3 postburn rats. SETTING: : Research laboratories in a medical center and an academic institution. SUBJECTS: Male Sprague-Dawley rats given sham treatment or treatment as a burn model with full-thickness skin scald over 30% total body surface area. CONCLUSIONS: We report (1) increased levels of neutrophil influx and extravasation in villi lamina propriae, including elastase-positive cells (postburn day 1), (2) heightened levels of intestinal myeloperoxidase activity (postburn day 3), (3) decreased levels of epithelial cell proliferation, migration, and E-cadherin (postburn day 3), and (4) increased enterocyte apoptosis and E. faecalis bacterial translocation (postburn day 3). Based on these structural and functional abnormalities, we propose a mechanism for burn injury-related intestinal barrier dysfunction that includes increased trans- and para-cellular leakage caused by impaired enterocyte renewal and decreased junctional E-cadherin levels subsequent to increased neutrophil influx and extravasation within the villus lamina propria microenvironment.

Animals↗
PubMed1990

Intestinal barriers to bacteria and their toxins.

Immunologic and nonimmunologic processes work together to protect the host from the multitude of microorganisms residing within the intestinal lumen. Mechanical integrity of the intestinal epithelium, mucus in combination with secretory antibody, antimicrobial metabolites of indigenous microorganisms, and peristalsis each limit proliferation and systemic dissemination of enteric pathogens. Uptake of microorganisms by Peyer's patches and other intestinal lymphoid structures and translocation circumvent the mucosal barrier, especially in immunosuppressed individuals. Improved understanding of the composition and limitation of the intestinal barrier, coupled with advances in genetic engineering of immunogenic bacteria, development of oral delivery systems, and immunomodulators, now make enhancement of mucosal barriers feasible.

Animals↗
PubMed1990

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↗
PubMedDate not supplied

Disruption of the small-intestine mucosal barrier after intestinal occlusion: a study with light and electron microscopy.

It is known that the gut may serve as a reservoir for various microorganisms, which under specific circumstances may intrude into the systemic circulation, causing systemic infections. The aim of the present study was to estimate the "critical time" of disruption of the small-intestine mucosal barrier in conditions of experimentally induced intestinal occlusion, based on the histopathological alterations observed under light and electron microscopy. Forty rabbits underwent small-intestine obstruction through ligation with a nonabsorbable suture. Blood cultures from portal vein and inferior vena cava, as well as cultures from the peritoneal fluid, a hepatic fragment, and a mesenteric lymph node, were obtained before the ligation (0 h). The same cultures were repeated at 4 and 8 h (group A, 20 rabbits) and at 6 and 12 h after the ligation (group B, 20 rabbits). Small-intestine specimens proximal to the occlusion were taken for examination under the optic and electronic microscope in the same time intervals. Five of 20 rabbits of group A died within 4 h and 6 of 20 rabbits of group B died within 6 h after the operation. All anaerobic cultures were negative. All aerobic cultures that became positive developed Escherichia coli colonies. Intestinal epithelium of dead animals was transformed to cuboid with destruction of goblet cells and alteration in secretion of acid polysaccharides. The mucosal appearance of all rabbits that survived 12 hours after ligation was the same. The disruption of the mucosal barrier begins 4 h after complete intestinal occlusion. At 12 h after complete intestinal occlusion, the disruption is total with different degrees of severity.

Animals↗
PubMed1996

Prophylactic administration of L-arginine improves the intestinal barrier function after mesenteric ischaemia.

BACKGROUND: Ischaemia/reperfusion (I/R) of the intestine causes mucosal injury associated with a high death rate in rats. AIM: To investigate whether nitric oxide (NO) might be implicated in the recovery of the intestinal mucosa after ischaemic insult. METHODS: Wistar rats were subjected to mesenteric artery occlusion for 90 minutes. The animals were given either L-arginine, the substrate of NO synthase, or molsidomine, a NO donor. The controls received casein hydrolysate. The compounds were administered by gavage 19, 16, and 1.5 hours before ischaemia. Mucosal barrier permeability and cGMP content were determined 24 hours after ischaemia. RESULTS: Survival after I/R was 50% in the control group. Animals treated with L-arginine or molsidomine exhibited a higher survival rate (70% and 83% respectively). Mucosal barrier permeability was decreased in rats receiving L-arginine or molsidomine compared with controls (4.0 (0.9) and 2.6 (0.6) v 11.2 (1.6) 14C-PEG pmol/segment, p < 0.05). Increased cGMP content was seen in the mucosa of the L-arginine group. CONCLUSION: The findings suggest that pretreatment with L-arginine or molsidomine ameliorates survival after intestinal I/R and improves mucosal barrier function.

Amino Acids, Essential↗
PubMed2005

Disordered enterocyte signaling and intestinal barrier dysfunction in the pathogenesis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in neonates, and is characterized by the development of diffuse intestinal necrosis in the stressed, pre-term infant. Systemic stress causes a breakdown in the intestinal mucosal barrier, which leads to translocation of bacteria and endotoxin and the initiation of a signaling response within the enterocyte. This review summarizes recent evidence defining a clear role that defective enterocyte signaling plays in the pathogenesis of NEC through the following mechanisms: 1) The localized production of nitric oxide by villus enterocytes results in an increase in enterocyte apoptosis and impaired proliferation; 2) The translocation of endotoxin results in a PI3K-dependent activation of RhoA-GTPase within the enterocyte leading to decreased enterocyte migration and impaired restitution; 3) Dysregulated sodium-proton exchange within the enterocyte by endotoxin renders the enterocyte monolayer more susceptible to damage in the face of the acidic microenvironment characteristic of systemic sepsis; and 4) Endotoxin causes a p38-dependent release of the pro-inflammatory molecule COX-2 by the enterocyte, which potentiates the systemic inflammatory response. An understanding of the mechanisms by which disordered enterocyte signaling contributes to the pathogenesis of barrier failure and NEC--through these and other mechanisms--may lead to the identification of novel therapeutic approaches for this devastating disease.

Bacterial Translocation↗