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At least 19 recordsLinked to original sources
PubMed2003

In vitro and in situ experimental model for X-ray microanalysis of intestinal epithelium.

Intestinal chloride (Cl) transport is disturbed in a number of diseases. X-ray microanalysis can be used to study the distribution of Cl and other ions in intestinal epithelial cells. In this study it was attempted to establish an experimental system that retains the in vivo elemental composition of intestinal epithelial cells. An in vitro system was set up in which a segment of rat intestine was mounted in a bath and perfused with different fluids. The chloride in the bath or in the perfusion fluid could be exchanged for gluconate or bromide to determine the direction of chloride fluxes. An in situ system was set up in which the animal was anesthetized and a segment of the intestine was perfused with different solutions. In the in vitro experiments the concentration of Na and Cl in the epithelial cells increased and that of K decreased. These changes occurred within the first 30 minutes of incubation. Uptake of chloride occurred mainly from the bath, as seen in experiments where bromide was used as a chloride analog. The concentration gradient between bath and tissue determined the extent of chloride uptake. Addition of glucose to the perfusion fluid and bath did not improve the results. In the in situ system, preservation of the intracellular ion composition was better. Acceptable results were obtained with perfusion with Krebs-Ringer's buffer without glucose for 30 minutes. In this case, the elemental content of the cell did not change appreciably during incubation. If glucose was added, the Na concentration increased in comparison to the control, both in crypt and villus cells. It is concluded that the intestinal epithelium is a sensitive system, very prone to disturbance of its homeostasis. However, the in situ system can be used in studies of agonist-induced ion transport.

Animals↗
PubMed2005

Rbm19 is a nucleolar protein expressed in crypt/progenitor cells of the intestinal epithelium.

Intestinal development and homeostasis rely on the coordination of proliferation and differentiation of the epithelium. To better understand this process, we are studying Rbm19, a gene expressed in the gut epithelium that is essential for intestinal morphogenesis and differentiation in the zebrafish (Development 130, 3917). Here we analyzed the expression of Rbm19 in several biological contexts that feature proliferation/differentiation cell fate decisions. In the undifferentiated embryonic gut tube, Rbm19 is expressed throughout the epithelium, but then becomes localized to the crypts of Lieberkühn of the adult intestine. Consistent with its expression in adult crypt/progenitor cells, expression is widespread in human colorectal carcinomas and dividing Caco-2 cells. Its expression in Caco-2 cells recapitulates the in vivo pattern, declining when the cells undergo confluence-induced arrest and differentiation. Rbm19 protein localizes to the nucleolus during interphase and to the perichromosomal sheath during mitosis, in accordance with the pattern described for other nucleolar proteins implicated in ribosome biogenesis. Interestingly, the loss of nucleolar rbm19, nucleolin/C23, and nucleophosmin/B23 in confluent Caco-2 cells did not signify loss of nucleoli as detected by electron microscopy. Taken together, these data point to the nucleolus as a possible locus for regulating the proliferation/differentiation cell fate decision in the intestinal epithelium.

Animals↗
PubMed1994

IL-4 directly modulates function of a model human intestinal epithelium.

Intestinal epithelia are in intimate contact with subepithelial and intraepithelial lymphocytes. When stimulated, mucosal lymphocytes generate inflammatory cytokines such as IL-4 and IFN-gamma. We have shown that IFN-gamma directly regulates epithelial function. It is unknown whether IL-4 might influence epithelial function and, if so, whether such influences are similar to or differ from those exerted by IFN-gamma. In this study, we examine the effect of human IL-4 on barrier function, ion transport, and immune accessory ligand expression on T84 cells, a crypt-like epithelial cell line. Basolateral exposure of epithelial monolayers to IL-4 attenuated epithelial barrier function by greater than 65% in a dose (50% of effective dose = 1 U/ml)- and time (t1/2 = 24 h)-dependent fashion, and was inhibitable by neutralizing anti-IL-4 and anti-IL-4R Ab. Stimulated Cl- secretion, as measured by epithelial short circuit current, was diminished by as much as 70% by IL-4. Epithelial preexposure to IL-4 brought about a greater than twofold increase in beta 2 integrin-dependent neutrophil adhesion to epithelial, but retarded neutrophil migration into and across epithelial monolayers. ELISAs revealed that epithelial exposure to IL-4 had no effect on cell surface expression of MHC class I, MHC class II, or ICAM-1. These results indicate that IL-4, like IFN-gamma, may serve to regulate intestinal epithelial function, but that resulting phenotypes may be cytokine specific. We speculate from these data that activation of the basolateral receptor for IL-4 potentially provides a new strategy for damping the cellular component of active inflammation in the intestine.

Cell Adhesion Molecules↗
PubMed1989

Plasma enteroglucagon, peptide YY and gastrin in rats deprived of luminal nutrition, and after urogastrone-EGF administration. A proliferative role for PYY in the intestinal epithelium?

Intestinal tissue mass was significantly reduced throughout the gastrointestinal tract (p less than 0.001) of intravenously fed (TPN) rats. Urogastrone-epidermal growth factor, (URO-EGF), reversed these changes. Although plasma enteroglucagon and gastrin levels showed a small increase with URO-EGF, this was far less than the gut tissue weight change, suggesting that it was unlikely that they were involved in modulating the proliferative response of the intestine to URO-EGF. Peptide tyrosine tyrosine (PYY) levels were however significantly increased by URO-EGF, indicating that PYY may possibly have a role in the modulation of intestinal cell proliferation.

Animals↗
PubMed1999

Expression and regulation of the human beta-defensins hBD-1 and hBD-2 in intestinal epithelium.

The intestinal epithelium forms a physical barrier to limit access of enteric microbes to the host and contributes to innate host defense by producing effector molecules against luminal microbes. To further define the role of the intestinal epithelium in antimicrobial host defense, we analyzed the expression, regulation, and production of two antimicrobial peptides, human defensins hBD-1 and hBD-2, by human intestinal epithelial cells in vitro and in vivo. The human colon epithelial cell lines HT-29 and Caco-2 constitutively express hBD-1 mRNA and protein but not hBD-2. However, hBD-2 expression is rapidly induced by IL-1alpha stimulation or infection of those cells with enteroinvasive bacteria. Moreover, hBD-2 functions as a NF-kappaB target gene in the intestinal epithelium as blocking NF-kappaB activation inhibits the up-regulated expression of hBD-2 in response to IL-1alpha stimulation or bacterial infection. Caco-2 cells produce two hBD-1 isoforms and a hBD-2 peptide larger in size than previously described hBD-2 isoforms. Paralleling the in vitro findings, human fetal intestinal xenografts constitutively express hBD-1, but not hBD-2, and hBD-2 expression, but not hBD-1, is up-regulated in xenografts infected intraluminally with Salmonella. hBD-1 is expressed by the epithelium of normal human colon and small intestine, with a similar pattern of expression in inflamed colon. In contrast, there is little hBD-2 expression by the epithelium of normal colon, but abundant hBD-2 expression by the epithelium of inflamed colon. hBD-1 and hBD-2 may be integral components of epithelial innate immunity in the intestine, with each occupying a distinct functional niche in intestinal mucosal defense.

Anti-Bacterial Agents↗
PubMed1978

Relationships between immunoglobulins and the intestinal epithelium.

The intestinal epithelium is intimately associated with immunoglobulins. This association may begin in neonatal life with the ingestion of large quantities of immunoglobulins in breast fluids. These ingested immunoglobulins probably have a local protective action in the intestinal lumen. In some mammalian species a large portion of the maternal immunoglobulins is translocated intact across the intestinal epithelium into the circulation, providing additional immunological protection. In rodents, the transepithelial translocation of IgG from breast fluids is initiated and critically dependent upon receptors on enterocyte surface membranes for the Fc region of IgG. Close epithelial-immunoglobulin relationships continue throughout life with the transfer of various classes of immunoglobulins across the epithelium into the intestinal fluids. In man and other mammalian species, IgA and IgM are selectively transported through enterocytes, principally in the crypts of intestinal glands. This transfer may involve binding of polymeric forms of these immunoglobulins to receptors on the abluminal surfaces of the enterocytes. The secretory component, a glycoprotein synthesized by enterocytes, may be such a receptor. IgE and IgG enter the gut lumen by mechanisms that are not defined but seem to be distinct from those involved in the translocation of IgA and IgM. Secreted antibodies in intestinal fluids and mucus bathe the luminal surfaces of intestinal epithelial cells but appear not to be firmly bound to their apical plasma membranes or glycocalyces. The intimate association of immunoglobulins with intestinal epithelial cells illustrates the close relationships that exist between the gut and lymphoid cells and their products. These relationships suggest the possibility that the gut epithelium is affected by a large variety of immunological reactions in health and disease; these possibilities, which have been explored only minimally, warrant much attention in the future. Studies on the binding, uptake, and intracellular transport of immunoglobulins by enterocytes could contribute much to the understanding of receptors for immunoglobulins on many other types of cells, such as lymphocytes, macrophages, mast cells, and the lining cells of placental or yolk sac membranes.

Animals↗
PubMed1982

[Unusual way of regenerating intestinal epithelium during seasonal intestinal transformation in Stichopus japonicus holothurians (possibility of an "external cambium")].

In Stichopus japonicus during summer months a profound morphofunctional rearrangement of the digestive tract resulting in its renovation is noted. It includes certain destructive-atrophic changes in the wall of the intestinal tube and some reparative processes accompanying them. In some species a spontaneous throwing out of the intestine with its subsequent restoration takes place. The mechanisms of the intestinal tube regeneration after its partial atrophy and after its spontaneous throwing out have much in common between them and with those previously described after an experimental throwing out. It is possible that under natural conditions (as well as under experimental ones) certain forms of wandering cells, migrating from the sublayers and/or from the surrounding structures (mesenterium and others), participate in the regenerative histogenesis of the intestinal epithelium. A suggestion is made that these cells are of coelomesodermal origin and play the role of the external cambium at sharp seasonal rearrangements of the holothurian intestinal tract.

Aging↗
PubMed1986

Effects of 30% intestinal resection on whole population cell kinetics of mouse intestinal epithelium.

The intestine remaining after resection undergoes a well known compensatory response. Crypts and villi grow in size, and the number of proliferating cells in a crypt increases. The crypt labeling index, however, is unchanged, which is thought to suggest that the growth fraction also remains unchanged and hence that the system is enlarged, but otherwise the new steady-state is similar to that of the controls. It is also generally accepted that no new crypts or villi are added to the adapting bowel. In this study we applied recently developed tools to study the response of the intestinal epithelium as a whole. Thus, the effects of 30% intestinal resection on whole population cell kinetics were determined by using flow cytometry, Coulter particle counting, and simple morphometric techniques. In addition to the classic response, we found an increase in the rate of crypt production, which was due mainly to a shorter crypt replication cycle. Thus, new crypts were produced at a faster rate in the resected animals than in the transected controls. This resulted in an expansion of the crypt cell population in the epithelium following resection. There was a corresponding expansion of the cycling cell population and thus an increase in the growth fraction of the resected epithelium. We conclude that for the crypt population, the classic story is correct with the exception that new crypts are added to the epithelium after resection. However, for the epithelium as a whole, the classic story is misleading as there appears to be an increase in the growth fraction of the epithelium after intestinal resection.

Animals↗
PubMed1995

T-lymphopoietic capacity of the mouse intestinal epithelium.

Small intestine intraepithelial lymphocytes (i-IELs) comprise a heterogeneous population of T cells that are part of the gut-associated lymphoid tissues. Recent studies indicate that murine i-IELs are greatly enriched for extrathymic T cells. Yet there is disagreement as to which i-IELS are extrathymic and which are not, and many aspects of intestinal T-cell development remain controversial. In this article, the developmental lineages of murine i-IELs are examined, and the thymopoietic potential of the intestine epithelium is discussed. A mechanism is described whereby all intestinal T cells develop extrathymically, and a concept of intestinal T cells is presented which suggests that lineages of i-IELs need to be viewed according to developmental factors exclusive of thymus dependency.

Animals↗
PubMed1982

The modulation by glucose transport of the electrical responses to hypertonic solutions of the goldfish intestinal epithelium.

Goldfish intestinal epithelium responds to mucosal hypertonicity with a negative biphasic transepithelial potential change and a relatively slow rise in transepithelial resistance, similar to that described for rabbit gallbladder (Wright et al. 1972; Smulders et al. 1972). In addition, the increase in resistance in goldfish intestine can be modulated by the presence or absence of glucose. E.g. during mucosal hypertonicity of 87 mosmoles/l the addition of 27.8 mmoles/l glucose to the serosal side further increased the resistance by 2.8 +/- 0.2 omega cm2, while mucosal addition reduced it by 11.2 +/- 2.6 omega cm2. Ouabain poisoning inverted this last response into a slowly and continuously rising resistance. The resistance response to mucosal glucose can be fully abolished by mucosal addition of phlorizin. The resistance change due to bilateral glucose addition is the sum of the separate mucosal and serosal responses. The effect of fructose at the serosal side resembles that of glucose added serosally; the mucosal effect of glucose could not be mimicked by fructose, but the decrease induced was of the same magnitude as the serosal effect of glucose, but of opposite sign. The effects of serosal addition of glucose and fructose and mucosal addition of fructose can be explained by different reflection coefficients of the cell membranes for glucose, fructose and mannitol. The mucosal effect of glucose is explained by a glucose-dependent influx of sodium at the mucosal side, stimulating a ouabain-sensitive pump at the baso-lateral aspects of the cell.

Animals↗
PubMed2005

Glutamine modulates LPS-induced IL-8 production through IkappaB/NF-kappaB in human fetal and adult intestinal epithelium.

The intestinal epithelium may serve as a nidus for inflammation that can cause local and systemic organ dysfunction. Relative to the adult, the immature intestine is exquisitely sensitive to inflammatory agents. Glutamine (Gln), an amino acid that is rapidly depleted during critical illness, modulates intestinal inflammation in vitro and in vivo. Here we relate Gln status to activation of the inhibitor of kappaB (IkappaB)/nuclear factor (NF)-kappaB signaling pathway in fetal-derived (H4) and adult (Caco-2) enterocytes. In the absence of Gln with or without LPS, H4 cells expressed more interleukin (IL)-8) than Caco-2 cells. Gln supplementation partially prevented the LPS-induced elevation of IL-8 in both cell types. IkappaBalpha was significantly decreased in both H4 and Caco-2 cells with Gln deprivation, and this was followed by an increase in NF-kappaB p65 in the nucleus. DNA binding of NF-kappaB was increased in both H4 and Caco-2 cells with Gln deprivation. IkappaBalpha phosphorylation was not altered by Gln status in either H4 or Caco-2 cells. Proteasomal inhibition after Gln depletion in Caco-2 cells was associated with an increase in the IkappaB-ubiquitin complex, but a decrease in complex formation in H4 cells, indicating that Gln deprivation alters IkappaBalpha through a pathway that differs from Caco-2 cells. We speculate that a reduced capacity of the immature enterocyte (H4) to respond to Gln deprivation with increased synthesis of IkappaBalpha rather than increased proteolysis as seen in the Caco-2 cells is the underlying mechanism.

Adult↗
PubMed2003

Live and let die in the intestinal epithelium.

The intestinal epithelium is a relatively simple developmental system and a prime example of tissue renewal from a source of multipotent stem cells. Throughout adulthood, intestinal epithelial proliferation, cell-fate specification and differentiation are coupled to migration in discrete units known as crypts of Lieberkühn. Physically guided by Eph receptors and their ligands, the ephrins, stem cell progeny transit through the proliferation/differentiation switch, and Notch diversifies their subsequent fates. Wnt signalling appears to control most of these events.

Animals↗
PubMed2005

Wnt control of stem cells and differentiation in the intestinal epithelium.

The intestinal epithelium represents a very attractive experimental model for the study of integrated key cellular processes such as proliferation and differentiation. The tissue is subjected to a rapid and perpetual self-renewal along the crypt-villus axis. Renewal requires division of multipotent stem cells, still to be morphologically identified and isolated, followed by transit amplification, and differentiation of daughter cells into specialized absorptive and secretory cells. Our understanding of the crucial role played by the Wnt/beta-catenin signaling pathway in controlling the fine balance between cell proliferation and differentiation in the gut has been significantly enhanced in recent years. Mutations in some of its components irreversibly lead to carcinogenesis in humans and in mice. Here, we discuss recent advances related to the Wnt/beta-catenin signaling pathway in regulating intestinal stem cells, homeostasis, and cancer. We emphasize how Wnt signaling is able to maintain a stem cell/progenitor phenotype in normal intestinal crypts, and to impose a very similar phenotype onto colorectal adenomas.

Animals↗
PubMed2002

Roles of the cytoskeleton and of protein phosphorylation events in the osmotic stress response in eel intestinal epithelium.

The eel intestinal epithelium responds to an acute hypertonic challenge by a biphasic increase of the rate of Cl(-) absorption (measured as short circuit current, Isc, and creating a negative transepithelial potential, V(te), at the basolateral side of the epithelium). While the first, transient phase is bumetanide-insensitive, the second, sustained phase is bumetanide-sensitive, reflecting activation of the apically located Na(+)-K(+)-2Cl(-) (NKCC) cotransporter, which correlates with the cellular RVI response. Here, we investigated the involvement of the cytoskeleton and of serine/threonine phosphorylation events in the osmotic stress-induced ion transport in the eel intestinal epithelium, focusing on the sustained RVI phase, as well as on the previously uncharacterized response to hypotonic stress. The study was carried out using confocal laser scanning microscopy, a quantitative F-actin assay, and transepithelial electrophysiological measurements (V(te) and Isc) in Ussing chambers. Hypertonic stress did not detectably alter either net F-actin content or F-actin organization. In contrast, a brief exposure to hypotonic stress decreased the total cellular F-actin content in eel intestinal epithelium by about 15%, detectable morphologically mainly as a decrease in the intensity of the apical brush border F-actin labeling.The bumetanide-sensitive response of V(te) and Isc to hypertonicity was potently inhibited by treatment with either cytochalasin, latrunculin A, colchicine, the protein kinase C (PKC) inhibitor chelerythrine, the myosin light chain kinase (MLCK) inhibitor ML-7, or the serine/threonine protein phosphatase inhibitor Calyculin A, but was unaffected by the PKA inhibitor H-89. The electrophysiological response of the epithelium to hypotonic stress was characterized by a sustained decrease of V(te) and Isc, which was smaller and recovered faster in the presence of either cytochalasin, latrunculin A, or colchicine. It is concluded that in eel intestinal epithelium, the changes in ion transport in response to both hyper- and hypotonic stress require the integrity of both F-actin and microtubules. In addition, the shrinkage-induced activation of NKCC appears to require the activity of both PKC and MLCK. It is suggested that NKCC regulation by hypertonic stress involves an interaction between the cytoskeleton and protein phosphorylation events.

Actins↗
PubMed1989

The interaction between plant lectins and the small intestinal epithelium: a primary cause of intestinal disturbance.

The literature concerning the effects of plant lectins on the small intestinal epithelium is reviewed. It appears that after oral intake, intact plant lectins can reach the small intestinal lumen. Their binding to the mucosal surface evokes an increased synthesis of glycoproteins and a degeneration of the intestinal epithelium. The epithelial alterations may result in hyperregenerative villus atrophy and endogenous nitrogen loss. These changes ultimately can lead to less efficient feed conversion, diminished growth, scouring, wasting and death. The possible significance of plant lectins in digestive disturbances in farm animals is suggested.

Animals↗
PubMed1986

Comparison of the effects of an ornithine decarboxylase inhibitor on the intestinal epithelium and on intestinal tumors.

Ornithine decarboxylase (ODC) catalyzes the rate-limiting step in the synthesis of polyamines, it has a short half-life, and its synthesis is under hormonal control. Recently, insight into the role of ODC and thus into the physiology of polyamines has been gained by the use of an inhibitor of ODC, difluoromethylornithine (DFMO). In the present report cell proliferation was measured by a stathmokinetic method in the crypt epithelium of the jejunum and colon of normal rats and in dimethylhydrazine-induced colonic tumors. Growth of human colon tumor xenografts in immunosuppressed mice and mouse colon tumor isografts was also assessed. Cell proliferation in primary colonic tumors was substantially suppressed by a single dose of DFMO at 100 mg/kg whereas the normal crypt epithelium of the small and large intestine required two doses at 400 mg/kg to produce a similar magnitude of inhibition of cell proliferation. DFMO was also found to suppress cell proliferation in, and the growth of, the transplantable colon cancers. Because of the apparent selectivity of the antimitotic activity of DFMO towards tumors, ODC inhibitors may prove to be useful anticancer drugs.

Animals↗