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PubMed1999

The impact of minor perioperative anesthesia-related incidents, events, and complications on postanesthesia care unit utilization.

UNLABELLED: The German Society of Anesthesiology and Intensive Care Medicine evaluates the standardized and routine reporting of perioperative anesthesia-related incidents, events, and complications (IEC). As part of the long-term project's definitions, IECs are graded according to severity and to their clinical consequence on further postanesthesia monitoring and treatment demands. The adult study population of our department comprised 37,079 patients recovering from anesthesia in a tertiary university hospital from July 1992 through June 1997. Cardiac, obstetric, craniotomy, thoracotomy, laparotomy, and emergency operations were excluded. Multivariate regression statistics were used to calibrate the impact of minor graded IECs on necessary postanesthesia care unit (PACU) utilization. Minor and severe IECs appeared in 22.1% and 0.2% of the patients. A minor IEC occurrence was a statistically significant (P < 0.001) predictor of PACU utilization in a multivariate regression model. The mean difference of PACU length of stay for patients with minor IECs was prolonged by a range of 6%-26% when adjusted for coexisting severity features such as age, gender, ASA physical status, and type and duration of anesthesia and surgery. We conclude that the IEC methodology integrates epidemiologic information about perioperative anesthesia outcome. Minor but frequently occurring IECs have an impact on PACU utilization and are thus important to measure and follow. IMPLICATIONS: It is desirable to know how anesthesia-related incidents, events, and complications influence postanesthesia care. Analyses of standardized and routine perioperative outcome data, as proposed by the German anesthesia quality project, can show that even minor events consume relevant resources and are thus important to measure and follow.

Adolescent↗
PubMed2002

Nitric oxide directly impairs intestinal barrier function.

Excess production of nitric oxide (NO) has been implicated in endotoxin-induced loss of gut barrier function in vivo. Thus, we tested the direct effect of NO on the barrier function of intestinal mucosal membranes suspended ex vivo in Ussing chambers and on IEC-6 enterocyte monolayers. In these experiments, ex vivo-mounted ileal membranes or IEC-6 cell enterocyte monolayers were exposed to the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP) over a dose range (10 microm to 2 mM) or medium. SNAP at concentrations of 1 or 2 mM, but not 10 or 100 microM, increased the rates of bacterial translocation (BT) across both the ileal membranes and the IEC-6 monolayers by >1 log (P < 0.05), as well as the permeability of the IEC-6 monolayers to phenol red (P < 0.05). The ileal membranes exposed to 1 or 2 mM SNAP for 3 h manifested histologic evidence of mucosal injury and decreases in electrical resistance and potential difference values (P < 0.05), while the IEC-6 cells exposed to SNAP for 18 h had increased levels of cell death (P < 0.05). Since NO produced locally by stimulated enterocytes could contribute to barrier dysfunction, NO production, iNOS mRNA levels, and monolayer permeability were measured in enterocytes (IEC-6 and Caco-2) exposed to medium, endotoxin (lipopolysaccharide [25 microg/mL]) or a cytokine mixture (IL-1beta 10 ng/mL, TNF-alpha 10 ng/mL, and INF-gamma 250 U/mL) for 6 or 24 h. Endotoxin increased NO production, iNOS mRNA expression, and monolayer permeability in the IEC-6, but not the Caco-2 cells, while exposure to the cytokine mixture increased both NO production, iNOS mRNA expression, and monolayer permeability in both the IEC-6 and Caco-2 cell lines. Based on the results of these studies it appears that NO can directly increase ileal mucosal membrane and enterocyte monolayer permeability and BT and that increased NO production and iNOS mRNA expression is associated with endotoxin- and/or cytokine-induced loss of enterocyte monolayer barrier function.

Animals↗
PubMed2004

Risk factors for cytomegalovirus viremia and disease developing after prophylaxis in high-risk solid-organ transplant recipients.

BACKGROUND: Cytomegalovirus (CMV) D+/R- solid-organ transplant (SOT) recipients carry increased risk of developing CMV disease; however, other risk factors in these patients have not been delineated. METHODS: We examined 20 demographic and clinical variables for their association with the development of CMV disease, as defined by an independent endpoint committee (IEC) and also by the investigator (investigator treated [IT]), or CMV viremia within 12 months of transplant in D+/R- transplant recipients who received prophylaxis with valganciclovir or oral ganciclovir for 100 days. RESULTS: Recipients with low creatinine clearance (Ccr,<40 mL/min) at screening had a significantly increased hazard of developing IEC-defined CMV disease (hazards ratio [HR]=4.28, confidence interval [CI] 1.69, 10.83). Females were twice as likely (HR=2.19, CI .21, 3.99) to develop IEC-defined CMV disease than males. These variables were associated with an increased risk of IEC-defined CMV disease in time-dependent models. Recipients with blood group A were also more likely to develop IEC-defined CMV disease than those with group O (HR=2.36 CI 1.24, 4.51) in the logistic regression model only. Prophylactic drug, organ type, recipient age, rejection episodes, and maintenance immunosuppression regimen were not associated with IEC-defined CMV disease. Female sex was the only variable associated with the development of CMV viremia (odds ratio [OR]=1.65; CI 1.03, 2.65) and IT CMV disease (OR=1.78; CI 1.08, 2.93). CONCLUSIONS: Low Ccr at screening and blood type A are risk factors for IEC-defined CMV disease, and female sex was a risk factor for IEC- and IT-defined CMV disease and viremia in high-risk SOT recipients. These variables should perhaps be considered when optimizing treatment.

ABO Blood-Group System↗
PubMed1995

Synthesis and regulation of accessory/proinflammatory cytokines by intestinal epithelial cells.

Intestinal epithelial cells (IEC) have been shown to act as antigen-presenting cells (APC) in vitro and may have this capacity in vivo. In order to determine whether IEC, like other APC, are able to produce accessory cytokines which may play a role in T cell activation, we assessed the accessory cytokine profile of IEC constitutively or after stimulation. We measured expression, production and regulation of accessory cytokines (IL-1 beta, IL-6, tumour necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta) by the presence of mRNA as well as secreted protein. Freshly isolated IEC from surgical specimens were cultured in the presence or absence of lipopolysaccharide (LPS), interferon-gamma (IFN-gamma), IL-1 beta or TNF-alpha. mRNA was assessed by a specific RNAse protection assay which controlled for contaminating cell populations while protein secretion was measured by ELISA (IL-1) or bioassay (TNF and IL-6). Neither IL-1 beta nor TNF-alpha were detectable in cultured IEC supernatants, supporting the lack of macrophage contamination. All IEC spontaneously secreted IL-6 at levels comparable to those of macrophages. IEC IL-6 mRNA also increased approximately 200-fold during the first 24 h of culture. LPS, IFN-gamma or TNF-alpha had no effect on spontaneous IL-6 production, and neither resulted in the secretion of IL-1 beta or TNF-alpha. However, IL-1 beta up-regulated IL-6 synthesis by 6-7-fold. IEC express a profile of cytokine mRNAs distinct from conventional APC (low level constitutive IL-6 expression but no detectable IL-1 beta, TGF-beta or TNF-alpha), adding to their uniqueness as APC.

Cytokines↗
PubMed1996

Effect of adherent Lactobacillus spp. on in vitro adherence of salmonellae to the intestinal epithelial cells of chicken.

Single strains of Lactobacillus acidophilus and Lact. fermentum, isolated from chicken intestine, were used to study in vitro interactions with Salmonella enteritidis, Salm. pullorum or Salm. typhimurium in an ileal epithelial cell (IEC) radioactive assay. Exclusion, competition and displacement phenomena were investigated by respectively incubating (a) lactobacilli and IEC together, prior to addition of salmonellae, (b) lactobacilli, IEC and salmonellae together, and (c) salmonellae and IEC, followed by the lactobacilli. Lactobacilli were selected for study because of their strong ability to adhere to IEC and poor aggregation with salmonellae. The results demonstrated that Lact. acidophilus significantly reduced (P < 0.05) the attachment of Salm. pullorum to IEC in the tests for exclusion and competition, but not in the displacement tests. Lactobacillus fermentum was found to have some ability to reduce the attachment of Salm. typhimurium to IEC under the conditions of exclusion (P < 0.08), competition (P < 0.09), but not displacement. However, both Lact. acidophilus and Lact. fermentum were unable to reduce the adherence of Salm. enteritidis to IEC under any of the conditions.

Animals↗
PubMed2002

Activation of K(+) channels and increased migration of differentiated intestinal epithelial cells after wounding.

Early mucosal restitution occurs by epithelial cell migration to reseal superficial wounds after injury. Differentiated intestinal epithelial cells induced by forced expression of the Cdx2 gene migrate over the wounded edge much faster than undifferentiated parental cells in an in vitro model. This study determined whether these differentiated intestinal epithelial cells exhibit increased migration by altering voltage-gated K(+) (Kv) channel expression and cytosolic free Ca(2+) concentration ([Ca(2+)](cyt)). Stable Cdx2-transfected IEC-6 cells (IEC-Cdx2L1) with highly differentiated phenotype expressed higher basal levels of Kv1.1 and Kv1.5 mRNAs and proteins than parental IEC-6 cells. Neither IEC-Cdx2L1 cells nor parental IEC-6 cells expressed voltage-dependent Ca(2+) channels. The increased expression of Kv channels in differentiated IEC-Cdx2L1 cells was associated with an increase in whole cell K(+) currents, membrane hyperpolarization, and a rise in [Ca(2+)](cyt). The migration rates in differentiated IEC-Cdx2L1 cells were about four times those of parental IEC-6 cells. Inhibition of Kv channel expression by polyamine depletion decreased [Ca(2+)](cyt), reduced myosin stress fibers, and inhibited cell migration. Elevation of [Ca(2+)](cyt) by ionomycin promoted myosin II stress fiber formation and increased cell migration. These results suggest that increased migration of differentiated intestinal epithelial cells is mediated, at least partially, by increasing Kv channel activity and Ca(2+) influx during restitution.

Animals↗
PubMed1998

Fas ligand- mediated killing by intestinal intraepithelial lymphocytes. Participation in intestinal graft-versus-host disease.

In vitro studies have demonstrated that intestinal intraepithelial lymphocytes (IEL) are constitutively cytotoxic; however, the mechanism and target of their cytotoxicity are unknown. Apoptosis of intestinal epithelial cells (IEC) and an increase in IEL numbers are classical signs of intestinal graft-versus-host disease (GVHD), although whether IEL can mediate IEC apoptosis directly in GVHD is unclear. Recent evidence suggests that target epithelial organ injury observed in GVHD is predominantly Fas-mediated; therefore, we investigated the possibility that IEL induce apoptosis of IEC through a Fas-mediated mechanism. Here, we demonstrate that the IEL isolated from normal mice readily display potent Fas ligand (FasL)-mediated killing activity after CD3 stimulation, and that IEC express Fas, suggesting that IEC are potential targets for FasL-mediated killing by IEL. In vitro, IEL isolated from GVHD mice have markedly increased FasL-mediated killing potential and are spontaneously cytolytic toward host-derived tumor cells predominantly through a Fas-mediated pathway. In vivo transfer of IEL isolated from GVHD mice induced significantly more IEC apoptosis in F1 wild-type mice than in Fas-defective F1lpr mice. Thus, these results demonstrate that FasL-mediated death of IEC by IEL is a major mechanism of IEC apoptosis seen in GVHD.

Animals↗
PubMed2006

Effect of recombinant human interleukin-11 on expressions of interleukin-11 receptor alpha-chain and glycoprotein 130 in intestinal epithelium cell line-6 after neutron irradiation.

AIM: To explore the effect of recombinant human interleukin-11 (rhIL-11) on the expressions of interleukin-11 receptor alpha-chain (IL-11Ralpha) and an additional signal transducer glycoprotein 130 (gp130) in intestinal epithelium cell line-6 (IEC-6) after neutron irradiation. METHODS: Cultured IEC-6 cells were exposed to 4.0Gy neutron and treated with 100 ng/mL rhIL-11 12 h prior to or immediately after irradiation. The apoptosis and necrosis rates and expressions of IL-11Ralpha and gp130 were observed by flow cytometry, immunohistochemistry, Western blot and image analysis. RESULTS: The apoptosis rate of IEC-6 cells was increased by irradiation at 6 h (P < 0.01), IL-11 stimulation resulted in a decreased apoptosis rate in irradiated IEC-6 cells (P < 0.05). In normal control IEC-6 cells, intense immunoreactivity of IL-11Ralpha was located within the cell membrane and cytoplasm. The level of IL-11Ralpha expression significantly decreased at 6 h after irradiation (P < 0.01) and restored at 24 h after irradiation. In IEC-6 cells treated with both radiation and rhIL-11, the level of IL-11Ralpha expression was higher than that of irradiated cells (P < 0.05). When it came to gp130 protein, it was located in the cytoplasm of IEC-6 cells. After irradiation, we found a progressive decrease in the expression of gp130 protein (P < 0.05) in 48 h post-radiation, while in rhIL-11-stimulated cells, it came back to normal level at 24 h after irradiation and decreased at 48 h, but was still higher than that of only irradiated cells (P < 0.05). CONCLUSION: rhIL-11 can protect IEC-6 cells from neutron irradiation. The protective effect of rhIL-11 might be connected with its ability to up-regulate the expressions of specific ligand-binding subunit IL-11Ralpha and signal-transducing subunit gp130.

Animals↗
PubMed2000

[Age-related changes in crossing over in Drosophila resemble the picture of interchromosomal effect of chromosome rearrangement on crossing over].

Crossing over in the left arm of chromosome 2 (2L) was studied in successive broods of Drosophila melanogaster females carrying intact chromosomes (+/+), inversion Muller-5 in the X chromosome (M-5/+), and insertion of the Y-chromosome material into region 34A (Is(2L)/+). The regions net-dp, dp-b, b-pr and pr-cn were examined in 14 two-day-old broods of females +/+ and M-5/+ and in 10 broods of females Is(2L)/+. In all lines, the highest level of crossing over was in the first three broods (eggs laid during the first 6 days of oviposition) and the lowest level in the broods 7-8 (eggs laid at days 14-16). A high rate of crossing over in the first broods of females +/+ and M-5/+ was due to an increment of exchanges in the proximal euchromatin regions (b-pr and pr-cn) and to an increase in the number of tetrads with double exchanges. These changes are similar to a pattern of the interchromosomal effect on crossing over (IEC) in structurally normal chromosomes. In Is(2L)/+ females, a high level of crossing over was due to extensive exchanges in the interstitial regions net-dp and dp and an increase in the number of tetrads with single exchanges. These changes resembled the IEC in rearranged chromosomes (in this case, in chromosomes bearing an insertion). Thus, the age changes of crossing over are similar to the consequences of the presence or absence of IEC. Age changes in crossing over in a chromosome depended both on the local rearrangements in this chromosome (the local effect on crossing over, LEC) and on rearrangements in nonhomologous chromosomes (IEC). In the first broods, both LEC and IEC decreased with an increase in the level of crossing over. In subsequent broods, the reduced level of crossing over was accompanied by an increase in both LEC and IEC. This suggests that the mechanisms responsible for the age changes in crossing over and IEC may have common steps. The contact model of crossing over may explain the similarity between the age changes in crossing-over and IEC. It is suggested that both phenomena result from delayed determination of crossing over in a meiotic cell. This may occur due to the retarded formation of the local contacts in one of the homologous chromosome pairs or because a higher number of local contacts is required to trigger crossing over in a meiotic cell (of early age).

Aging↗
PubMed2002

[Effects of exogenous nucleotides on the proliferation and migration of intestinal epithelial cells].

The effect of exogenous nucleotides on proliferation and migration of a normal rat small intestinal epithelial cell line IEC-6 is studied. The concentration-effects as well as interaction of exogenous nucleotides on proliferation of IEC-6 are measured by MTT. Migration of IEC-6 after wounded is determined by an in vitro model of intestinal epithelial restitution of IEC-6 monolayer. Expression of TGF beta is detected by immunohistochemistry. The results show AMP and GMP remarkably inhibit proliferation of IEC-6 in concentration-dependent manner respectively at 30 mumol/L or 150 mumol/L and more. CMP, UMP and nucleotides mixture can not enhance or inhibit the growth with the exception of inhibition of CMP on proliferation at very high concentration (1440 mumol/L). In contrast, CMP, especially UMP, can remarkably abolish the proliferation-inhibiting effects of AMP or GMP on the cell, when AMP or GMP is supplemented. Nucleotides mixture significantly facilitate migration of IEC-6 after wounded but fail to promote the expression of TGF beta. It is concluded that purine nucleotides inhibits proliferation of IEC-6. Pyrimidine nucleotides can abolish the inhibitive effects of purine nucleotides, and Nucleotides mixture promotes migration of IEC-6 after wounded by a TGF beta-independented way.

Animals↗
PubMed1981

Cytotoxic effects and metabolism of benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene in duodenal and ileal epithelial cell cultures.

Two epithelial cell lines have been established from the duodenum (IEC-17) and the ileum (IEC-18) of outbred germfree Crl:CD(SD)GN rats. They have a very similar morphology and ultrastructure, a normal rat diploid karyotype, comparable growth rates, and a similar set of surface antigens as detected with monoclonal antibodies specific for intestinal epithelial cell surface proteins in vivo. Both cell lines do not grow in soft agar and when injected into syngeneic animals do not form tumors. The toxic effects of benzo[a]pyrene (BP) and 7,12-dimethylbenz[a]anthracene (DMBA) were studied in these two cell lines. The IEC-18 cells were found to be much more sensitive to both chemicals than the IEC-17 cells. In particular, at concentrations greater than 1 microgram/ml, DMBA completely and irreversibly inhibited cell proliferation in the IEC-18 cells, whereas it produced a less marked and reversible inhibition in the IEC-17 cells. The metabolism of BP and DMBA to water-soluble products was studied; BP was apparently metabolized at similar rates in the two cell lines, whereas a striking difference was observed with DMBA, which was metabolized at a rate 10-15 times greater in the IEC-18 cells than that in the IEC-17 cells. These results suggest that cultured cell lines derived from different portions of the intestinal tract have similar properties in vitro, but they may have very different responses to chemical carcinogens.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Effect of heat shock and endotoxin stress on enterocyte viability apoptosis and function varies based on whether the cells are exposed to heat shock or endotoxin first.

BACKGROUND: Stress-gene responses, including the heat shock (HS) response and the acute phase response, are protective mechanisms for cells after exposure to stress. Both responses cannot occur simultaneously, and, in endothelial cells, the sequence of stress-gene expression seems to be a critical factor in whether cellular protection or injury occurs. OBJECTIVE: To determine if the sequence of stress-gene expression affects cellular protection or injury in epithelial cells. DESIGN: Randomized controlled in vitro study. SETTING: University research laboratory. SUBJECTS: Rat intestinal epithelial cell-6 (IEC-6) cells were grown on 35-mm culture dishes, chamber slides, or in a bicameral system to confluence or until tight junction integrity was established. INTERVENTIONS: Rat IEC-6 cells were examined for viability, apoptosis, and bacterial translocation (BT) after exposure to 25-micrograms/mL lipopolysaccharide (LPS) for 18 hours to HS (43 degrees C) for 90 minutes, to LPS followed by HS, or to HS followed by LPS. MAIN OUTCOME MEASURES: The IEC-6 cells were stained for viability and apoptosis using trypan blue and a direct immunoperoxidase detection of digoxigenin-labeled genomic DNA (Apop Tag Plus In Situ Apoptosis Detection Kit, Oncor, Gaithersburg, Md), respectively. Bacterial translocation was measured by culturing the bacteria (ie, Escherichia coli) that crossed the IEC-6 cell monolayer in the bicameral system. RESULTS: Control cells (medium only) and cells exposed to LPS alone, HS alone, or HS followed by LPS had a viability from 92% to 98%, and the percentage of apoptotic cells ranged from 2.2% to 5.7%. In contrast, IEC-6 cells exposed to LPS followed by HS had a significantly lower viability (83%, P < .05 vs all other groups) and a higher percentage of apoptotic cells (12.2%, P < .01). At 3 hours after challenge with E coli, the LPS-exposed IEC-6 cell monolayers had significantly increased BT vs control monolayers (P < .05), while the IEC-6 cell monolayers exposed to HS followed by LPS had decreased BT (P < .05). Conversely, cells exposed to LPS followed by HS had the highest magnitude of BT (P < .01 vs all other groups). CONCLUSIONS: These results indicate that preinduction of HS response can diminish LPS-induced cell injury, while induction of HS response after the LPS challenge (ie, the acute phase response) may lead to decreased enterocyte viability, increased apoptosis, and cellular dysfunction as manifested by BT.

Acute-Phase Reaction↗
PubMed2006

RNA interference reveals a differential role of FAK and Pyk2 in cell migration, leading edge formation and increase in focal adhesions induced by LPA in intestinal epithelial cells.

In the gastrointestinal mucosa, cell migration plays a crucial role in the organization and maintenance of tissue integrity but the mechanisms involved remain incompletely understood. Here, we used small-interfering RNA (siRNA)-mediated depletion of focal adhesion kinase (FAK) protein to determine the role of FAK in wound-induced migration and cytoskeletal organization in the non-transformed intestinal epithelial cells IEC-6 and IEC-18 stimulated with the G protein-coupled receptors (GPCR) agonist lysophosphatidic acid (LPA). Treatment of these cells with FAK siRNA substantially reduced FAK expression, but did not affect the expression of proline-rich tyrosine kinase 2 (Pyk2). Knockdown of FAK protein significantly inhibited LPA-induced migration of both IEC-18 and IEC-6 cells. LPA induced reorganization of actin and microtubule cytoskeleton in the leading edge was largely inhibited in FAK siRNA-transfected IEC-18 cells. Interestingly, in contrast to the FAK-/- cells, which exhibit an increased number of prominent focal adhesions when plated on fibronectin, FAK knockdown IEC-18 cells exhibited dramatically decreased number of focal adhesions in response to both LPA and fibronectin as compared with the control cells. We also used siRNAs to knockdown Pyk2 expression without reducing FAK expression. Depletion of Pyk2 did not prevent LPA-induced migration or cytoskeletal reorganization in IEC-18 cells. In conclusion, our study shows that FAK plays a critical role in LPA-induced migration, cytoskeletal reorganization, and assembly of focal adhesions in intestinal epithelial cells whereas depletion of Pyk2 did not interfere with any of these responses elicited by LPA.

Cell Line↗
PubMed1998

Regulation of mucosal B cell immunoglobulin secretion by intestinal epithelial cell-derived cytokines.

Intestinal epithelial cells (IEC) secrete a variety of cytokines and, because of their close proximity to B cells in the lamina propria, may affect local antibody production via these cytokines. However, studies have not yet addressed which and to what extent these IEC-derived cytokines may affect B cell antibody production. In this study, rat mesenteric lymph node B cells were cultured with culture supernatants from the rat IEC-6 intestinal epithelial cell line to determine their effect on immunoglobulin (Ig) secretion. Unstimulated IEC-6 cells were found to secrete sufficient levels of IL-6 to enhance IgA, IgG and IgM secretion by unstimulated B cells. However, culture of lipopolysaccharide (LPS)-stimulated B cells with the unstimulated IEC-6 supernatant resulted in an enhancement of IgA secretion while IgM secretion was significantly suppressed. Depletion of the IEC-6 supernatant using cytokine specific antibodies revealed that both interleukin 6 (IL-6) and transforming growth factor beta (TGF-beta) were responsible for the enhanced IgA secretion while TGF-beta suppressed IgM secretion. More importantly, culture supernatants from LPS stimulated IEC-6 cells contained enhanced levels of IL-6 which enhanced both IgG and IgA production and partially overcame the suppressive effect of TGF-beta on IgM secretion. These results suggest that intestinal epithelial cells may secrete IL-6 and TGF-beta to regulate local B cell antibody secretion and their effect may be highly dependent upon the activation state of the epithelial cells.

Animals↗
PubMed1997

The intestinal epithelial cell: immunological aspects.

IECs likely play an important role in immunological defense mechanism. Apart from being a passive barrier against luminal bacteria, IECs secrete protective and microbiocidal products such as ITF, complement components and cryptdins into the lumen. Moreover, IECs produce secretory component that is essential for the transport of IgA from the lamina propria into the lumen. IECs also have regulatory functions. They express adhesion molecules important in the homing of T cells and other leukocytes, and likely modulate T cell functions in a paracrine way. Furthermore, IECs secrete cytokines, either constitutively or after bacterial challenge, and they express cytokine receptors. Lastly, IECs may play an important role as non-professional antigen-presenting cells by expressing classical MHC class I and class II and nonclassical MHC class I molecules on the cell surface. This aspect is particularly intriguing in that IECs also express a FcR that may have a function in luminal antigen sampling.

Animals↗
PubMed2001

Influence of fatty alcohol and other fatty acid derivatives on fatty acid uptake into rat intestinal epithelial cells.

We investigated the influence of various substrates on the uptake of long-chain fatty acid into IEC-6, rat intestinal epithelial cell line. The uptake of [3H]oleic acid into IEC-6 cells was a saturable function of the oleic acid concentration. Long-chain fatty acids significantly inhibited the oleic acid uptake into IEC-6 cells and shorter-chain fatty acids had little or no effect. Various fatty acid esters suppressed the oleic acid uptake into IEC-6. Fatty alcohols also inhibited oleic acid uptake into IEC-6 and the length of the carbon chain played an important role. These results suggest that long-chain fatty acid uptake was inhibited by the substrates which had a structure similar to long-chain fatty acids, especially those with a long carbon chain. At least two molecules, fatty acid translocase and fatty acid transport protein type 4, which are considered to be involved in the long-chain fatty acid transport into the cell, were expressed on IEC-6 cells, supporting the existence of the carrier-mediated system of long-chain fatty acid transport on IEC-6 cells.

Animals↗
PubMed2005

Effects of azathioprine and its metabolites on repair mechanisms of the intestinal epithelium in vitro.

Erosions and ulcerations of the intestinal epithelium are hallmarks of inflammatory bowel diseases (IBD). Intestinal epithelial cell migration (restitution) and proliferation are pivotal mechanisms for healing of epithelial defects after mucosal injury. In addition, the rate of apoptosis of epithelial cells may modulate intestinal wound healing. The purine antagonists azathioprine (AZA) and 6-mercaptopurine (6-MP) are widely used drugs in the treatment of IBD. In the present study, the hitherto unknown effects of AZA as well as its metabolites 6-MP and 6-thioguanine (6-TG) on repair mechanisms and apoptosis of intestinal epithelia were analysed. Intestinal epithelial cell lines (human Caco-2, T-84 and HT-29 cells, rat IEC-6 cells) were incubated with AZA, 6-MP or 6-TG for 24 h (final concentrations 0.1-10 microM). Migration of Caco-2 and IEC-6 cells was analysed by in vitro restitution assays. Caco-2 and IEC-6 cell proliferation was evaluated by measurement of [3H]thymidine incorporation into DNA. Apoptosis of Caco-2, T-84, HT-29 and IEC-6 cells was assessed by histone ELISA, 4'6'diamidino-2'phenylindole-dihydrochloride staining as well as flow cytometric analysis of Annexin V/propidium iodide (PI)-stained cells. Cell cycle progression was evaluated by PI staining and flow cytometry. Epithelial restitution was not significantly affected by any of the substances tested. However, proliferation of intestinal epithelial cells was inhibited in a dose-dependent manner (maximal effect 92%) by AZA, 6-MP as well as 6-TG. In HT-29 cells, purine antagonist-effected inhibition of cell proliferation was explained by a cell cycle arrest in the G2 phase. In contrast, AZA, 6-MP and 6-TG induced no cell cycle arrest in Caco-2, T-84 and IEC-6 cells. AZA, 6-MP as well as 6-TG induced apoptosis in the non-transformed IEC-6 cell line but not in human Caco-2, T-84 and HT-29 cells. In summary, AZA and its metabolites exert no significant effect on intestinal epithelial restitution. However, they profoundly inhibit intestinal epithelial cell growth via various mechanisms: they cause a G2 cell cycle arrest in HT-29 cells, induce apoptosis in IEC-6 cells and dose-dependently inhibit intestinal epithelial proliferation.

Animals↗
PubMed2003

Apc+/Min colonic epithelial cells express TNF receptors and ICAM-1 when they are co-cultured with large intestine intra-epithelial lymphocytes.

Adenomatous polyposis coli (APC) functions are involved in the heterotypic interactions occurring between intestinal epithelial cells (IECs) and intra-epithelial lymphocytes (IELs). These interactions may be of interest in cancer prevention, since recent data provide evidence for lymphocyte mediated immunosurveillance of epithelial cancers. The present study attempts to determine if APC inactivation induces changes in the cross-talk between IEC and large intestine IEL (LI-IEL) through intercellular adhesion molecule (ICAM-1)/leukocyte function-associated (LFA-1) interactions. Mouse Apc+/+ and Apc+/Min colonocytes were co-cultivated with LI-IEL. When co-cultured with LI-IEL Apc+/Min IEC but not Apc+/+ IEC expressed high levels of ICAM-1. The presence of ICAM-1 was linked to TNFalpha production in both co-cultures and TNFR expression only in co-cultivated Apc+/Min IEC. Finally, butyrate enhanced the expression of ICAM-1 in Apc+/Min IEC co-cultured with LI-IEL, and the secretion of TNFalpha by both types of co-cultures. These events could participate in determining the Apc+/Min IEC immunogenicity under different in vivo conditions.

Animals↗