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PubMed2006

Breakdown of intestinal mucosa via accelerated apoptosis increases intestinal permeability in experimental severe acute pancreatitis.

BACKGROUND: Bacterial translocation plays an important role for infectious complications in severe acute pancreatitis (SAP). Breakdown of intestinal mucosal integrity may increase intestinal permeability and may be implicated in bacterial translocation. It is suggested that increase in intestinal permeability is correlated with the changes of tight junction and/or apoptosis in intestinal epithelial cells. The aim of this study was to investigate the changes of intestinal mucosa and its permeability in SAP. METHODS: SAP was induced by injection of 3% sodium deoxycholate into the biliopancreatic ducts in rats. Permeability of intestinal wall was assayed ex vivo by measuring the leaked amount of FITC-dextran from the ileum pouch. Alteration of tight junction proteins such as zonula occludens (ZO)-1 and Occludin was evaluated by Western blotting and immunofluorescence staining. Apoptotic change of intestinal mucosa was detected by TUNEL staining and DNA fragmentation ELISA. In vitro, apoptosis-inducing effect of pancreatitis-associated ascitic fluid (PAAF) was examined using T84 cells. Integrity of monolayer cells was assessed by transepithelial electric resistance (TEER). RESULTS: Permeability of ileum was significantly increased 6 h after induction of SAP. Blood endotoxin level was significantly elevated and bacterial translocation occurred 18 h after induction of SAP. Six hours after induction of SAP, expressions of ZO-1 and Occludin were not altered, but apoptosis of ileum mucosa was significantly accelerated. Addition of PAAF to T84 cells did not affect expressions of ZO-1 or Occludin, but significantly increased the apoptosis and significantly decreased TEER. CONCLUSIONS: These results suggest that breakdown of intestinal mucosa via accelerated apoptosis may increase in intestinal permeability in SAP and that PAAF contains factor(s) that accelerates the apoptosis of intestinal epithelial cells.

Animals↗
PubMed2006

Role of nucleotide excision repair deficiency in intestinal tumorigenesis in multiple intestinal neoplasia (Min) mice.

Mice deficient in the Xeroderma pigmentosum group A (Xpa) gene are defective in nucleotide excision repair (NER) and highly susceptible to skin carcinogenesis after dermal exposure to UV light or chemicals. Min (multiple intestinal neoplasia) mice, heterozygous for a germline nonsense mutation in the tumor suppressor gene adenomatous polyposis coli (Apc), develop intestinal tumors spontaneously and show additional intestinal tumors after exposure to the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). In this study, we investigated the impact of loss of XPA function on PhIP-induced intestinal tumorigenesis in F1 offspring of Min/+ (Apc(+/-)) mice crossed with Xpa gene-deficient mice. Apc(+/-) mice lacking both alleles of Xpa had higher susceptibility towards toxicity of PhIP, higher levels of PhIP-DNA adducts in the middle and distal small intestines, as well as in liver, and a higher number of small intestinal tumors at 11 weeks, compared with Apc(+/-) mice with one or two intact Xpa alleles. Localization of tumors was not affected, being highest in middle and distal small intestines in all genotypes. At 11 weeks of age, the number of spontaneous intestinal tumors was not significantly increased by homozygous loss of Xpa, but untreated Apc(+/-)/Xpa(-/-) mice had significantly shorter life-spans than their XPA-proficient littermates. Heterozygous loss of Xpa did not affect any of the measured end points. In conclusion, the Xpa gene and the NER pathway are involved in repair of bulky PhIP-DNA adducts in the intestines and the liver, and most probably of DNA lesions leading to spontaneous intestinal tumors. These results confirm a role of the NER pathway also in protection against cancer in internal organs, additional to its well-known importance in protection against skin cancer. An effect of Apc(+/-) on adduct levels, additional to that of Xpa(-/-), indicates that the truncated APC protein may affect a repair pathway other than NER.

Animals↗
PubMed1988

Morphologic and nutritional responses to intestinal patching following intestinal resection.

Growth of neomucosa has been investigated as a means to increase intestinal surface area in the short-bowel syndrome. Functional neomucosa grows over patched intestinal defects, but the effect of the patching procedure on absorption is unknown. The purpose of this study was to determine morphologic and nutritional responses to intestinal patching after resection. Fifteen dogs (13 to 19 kg) underwent either 75% resection of the small intestine (control group, n = 5), simultaneous resection and patching of the intestinal remnant with colon serosa (simultaneous group, n = 5), or resection with patching 12 weeks later (delayed group, n = 5). Caloric intake was standard in the three groups. Animals were killed 40 weeks after resection or patching. At that time, defects were 95% covered with neomucosa in both patched groups. Intestinal remnant length increased significantly in controls (139 +/- 20% initial length) compared to the simultaneous group (99 +/- 6%, p less than 0.05) but not to the delayed group (119 +/- 11%). Villous height of intestinal mucosa was greater in the control and delayed groups than in the simultaneous group (714 +/- 36 and 624 +/- 111 versus 535 +/- 54 micron, p less than 0.05). Fasting gastrin levels were significantly greater in patched animals than after resection alone (p less than 0.05). Intestinal transit by barium meal was significantly longer in patched animals (18 +/- 7 minutes versus 11 +/- 6, p less than 0.05). Body weight and serum albumin level were significantly lower in patched animals at death. Fecal weight, moisture, and fat excretion were significantly increased in the simultaneous group. Although intestinal patching results in the growth of neomucosa and prolonged transit time, it has a deleterious effect on absorption and nutritional status. In part, this may be related to inhibition of intestinal adaptation and gastric hypersecretion in patched animals.

Animals↗
PubMed1993

Influence of fatty acid absorption on bidirectional release of immunoglobulin A into intestinal lumen and intestinal lymph in rats.

Effects of absorption of long and middle chain fatty acids on IgA secretion into the intestinal lumen and intestinal lymph and the factors which evoke changes in IgA secretion during the absorptive process were examined in rat small intestine. Bidirectional secretion of IgA from the intestinal mucosa into the intestinal lumen and intestinal lymph was continuously observed in the control condition. Perfusion of oleic acid (a long-chain fatty acid) micelle into the jejunal loop induced a significant increase in IgA output into the intestinal lymph. In contrast, lymphatic output of IgA was significantly decreased when oleic acid micelle was administered intraduodenally. Absorption of octanoic acid, a middle-chain fatty acid, did not produce any significant changes in IgA output into either direction. CR1505, a CCK-receptor antagonist, significantly attenuated the oleic acid-induced increase in IgA secretion into the intestinal lumen, but did not affect the oleic acid-induced decrease in lymphatic IgA secretion. Pluronic L-81, an inhibitor of chylomicron formation and secretion, significantly attenuated the decrease in IgA output into the intestinal lymph during oleic acid absorption without affecting the luminal IgA output. The rate of release of IgA into the intestinal lumen is stimulated by absorption of long-chain fatty acids possibly through the influence of locally released CCK, while the transport process of IgA into lymphatics is controlled by a different mechanism which is closely correlated with the intracellular formation and secretion of chylomicron.

Animals↗
PubMed1996

Expression of mRNA for vasoactive intestinal peptide in rat small intestine.

Transplantation of small intestine is a neural model that permits studies of expression of the neuropeptide, vasoactive intestinal peptide, following extrinsic denervation, transection of intrinsic neural pathways, and an ischemic interval. Tissue levels of vasoactive intestinal peptide were examined at 3 months in ileum from a sham operation, in ileum after resection of proximal small intestine, in ileum after resection of proximal small intestine and extrinsic denervation, in ileum after resection of proximal small intestine and 30 min of ischemia, and in ileum obtained 3 months after ileal isografting in Lewis-to-Lewis combinations. Vasoactive intestinal peptide levels were increased in transplanted rat ileum, resection controls, denervation controls, and ischemic controls compared to sham-operated ileum (pANOVA < 0.01). The increased levels of this peptide were highest in denervation controls and lowest in ischemic controls. Northern blot analysis using rat vasoactive intestinal peptide cDNA identified a single 1.7-kb transcript in normal and transplanted rat ileum. The density of vasoactive intestinal peptide transcripts was increased in transplanted ileum (8450 +/- 540) compared to normal ileum (5790 +/- 620) (P < 0.01), and the ratio of this transcript to glyceraldehyde-3-phosphate dehydrogenase density units was also increased in transplanted ileum (0.81 +/- 0.08) compared to normal ileum (0.40 +/- 0.07; P < 0.01). Enhanced transcriptional regulation was the likely mechanism for increased tissue vasoactive intestinal peptide. The increased tissue levels appeared to be a response to extrinsic denervation and transection of intrinsic neural pathways, while an ischemic interval appeared to decrease tissue levels of the peptide.

Animals↗
PubMed2001

Body and intestinal growth of broiler chicks on a commercial starter diet. 1. Intestinal weight and mucosal development.

1. A study was conducted on the pattern of development of the intestinal mucosa of the Steggles x Ross (F1) strain of broiler chickens reared on a commercial starter diet. The mechanisms underlying the structural changes were also assessed. 2. In relation to body weight, small intestinal weight peaked at 7 d of age and declined subsequently. There was also a reduction in the relative weights of the gizzard and yolk sac with age. The length of the small intestine and its regions increased with age. 3. Crypt depth increased with age in the duodenum and jejunum while villus height increased significantly with age in all three regions of the small intestine. There were also significant changes in apparent villus surface area in the three regions, while interactions between age and intestinal region were significant in the case of crypt depth and villus height. 4. There were significant differences between the age groups in the mucosal protein content of jejunal and ileal homogenates, both tending to peak at 7 d of age. The DNA content of the intestinal mucosa declined with age in the three regions of the small intestine. While there was an increase in RNA content in the duodenum and ileum, there was a reduction in the jejunum. 5. Protein: DNA ratio increased between hatch and 21 d of age in all intestinal regions. Protein: RNA ratio decreased with age in the duodenum and ileum but increased in the jejunum. There were significant increases in RNA: DNA ratio in the duodenum and ileum but no changes were observed in the jejunum. The interactions between age and intestinal region were significant for all biochemical indices assessed. 6. At all ages, enterocyte proliferation at the jejunum was completed and quantifiable within 1 h of administration of 5-bromo-2'-deoxyuridine (BrDU). Subsequent assessment revealed an increase in crypt column count and number of BrDU-labelled cells. The rate of cell migration increased with age while there was a decline in the distance migrated in proportion to mucosal depth. The estimated life-span of enterocytes and time spent by enterocytes in the crypt varied with age. In d-old and 7-d-old chicks, migration was complete or nearly complete within 96 h of cell birth. 7. Although the intestinal mucosa of the strain was structurally developed at hatch, there was much change in structure with age, especially over the first 7 d post hatch. The rate of development was most rapid in the jejunum but the other regions are also important, on account of villus height or relative length of the region.

Age Factors↗
PubMed1998

Intestinal handling of mercury in the rat: implications of intestinal secretion of inorganic mercury following biliary ligation or cannulation.

Three sets of experiments were carried out to determine if there is an intestinal secretory component in the fecal excretion of administered inorganic mercury. In the first set of experiments the disposition of a nontoxic 0.5-micromol/kg intravenous dose of inorganic mercury was evaluated in control rats and rats whose bile duct had been ligated. Data collected 24 h after the administration of mercuric chloride indicated that some inorganic mercury had moved from the blood across the epithelium into the lumen of the stomach, small intestine, and large intestine. This secretory movement of mercury was most prominent in the small intestine. Interestingly, the renal uptake and accumulation of mercury were diminished significantly in the rats whose bile duct had been ligated. A time-course experiment showed that the maximum amount of secretory movement of mercury into the lumen of the small intestine occurred during the initial 12 h after the injection of mercuric chloride. By the end of 24 h after the injection of mercuric chloride, much of the inorganic mercury secreted in the small intestine appeared to have moved down into the large intestine. In a third experiment, the disposition of mercury was evaluated in control rats and rats who had their bile duct cannulated. The rationale for this third experiment was to study the disposition of mercury under conditions where obstruction of biliary outflow from the liver would not be as much of an issue as with ligation of the bile duct. Evidence for movement of mercury into the lumen of the intestines was also obtained from the rats whose bile duct had been ligated. Eighteen hours after the injection of mercuric chloride the amount of mercury in the luminal compartment of the small intestine was not statistically different between the two groups of rats. Approximately 1.7-2.1% of the administered dose was present in the luminal contents of the small intestine. Decreased renal uptake of mercury was also detected in the rats whose bile duct had been cannulated. The findings from the present study show that when bile flow is obstructed or diverted, clear evidence for secretory movement of mercury into the lumen of the gastrointestinal (GI) tract can be demonstrated. These findings also indicate that the secretory movement of mercury into the lumen of the GI tract is a mechanism that contributes significantly to the pool of mercury that is excreted in the feces.

Animals↗
PubMedDate not supplied

Intestinal transplantation in pediatric patients: a nursing challenge: Part One: Evaluation for intestinal transplantation.

Intestinal transplantation offers hope to children with intestinal failure and life-threatening complications of parenteral nutrition (PN). As more transplant centers are adding intestinal transplantation to their existing programs, new challenges are presented to nursing professionals. This three-part series will provide information for nursing professionals regarding evaluation for intestinal transplantation, donor preparation, the surgical procedure, immediate postoperative care of the transplant recipient, complications of intestinal transplantation, and long-term care of the intestinal transplant patient. Part 1 will discuss the indications for intestinal transplantation, the evaluation of patients for intestinal transplantation, the process of listing patients for intestinal transplantation, and the waiting time for donor organs for intestinal transplantation. The information presented represents the approach taken at University of Nebraska Medical Center.

Child↗
PubMed2001

The role of small intestinal bacterial overgrowth, intestinal permeability, endotoxaemia, and tumour necrosis factor alpha in the pathogenesis of non-alcoholic steatohepatitis.

BACKGROUND: Small intestinal bacterial overgrowth may contribute to the development of non-alcoholic steatohepatitis, perhaps by increasing intestinal permeability and promoting the absorption of endotoxin or other enteric bacterial products. AIMS: To investigate the prevalence of small intestinal bacterial overgrowth, increased intestinal permeability, elevated endotoxin, and tumour necrosis factor alpha (TNF-alpha) levels in patients with non-alcoholic steatohepatitis and in control subjects. PATIENTS AND METHODS: Twenty two patients with non-alcoholic steatohepatitis and 23 control subjects were studied. Small intestinal bacterial overgrowth was assessed by a combined (14)C-D-xylose and lactulose breath test. Intestinal permeability was assessed by a dual lactulose-rhamnose sugar test. Serum endotoxin levels were determined using the limulus amoebocyte lysate assay and TNF-alpha levels using an ELISA. RESULTS: Small intestinal bacterial overgrowth was present in 50% of patients with non-alcoholic steatosis and 22% of control subjects (p=0.048). Mean TNF-alpha levels in non-alcoholic steatohepatitis patients and control subjects were 14.2 and 7.5 pg/ml, respectively (p=0.001). Intestinal permeability and serum endotoxin levels were similar in the two groups. CONCLUSIONS: Patients with non-alcoholic steatohepatitis have a higher prevalence of small intestinal bacterial overgrowth, as assessed by the (14)C-D-xylose-lactulose breath test, and higher TNF-alpha levels in comparison with control subjects. This is not accompanied by increased intestinal permeability or elevated endotoxin levels.

Adult↗
PubMed2003

Dopamine-induced protection against indomethacin-evoked intestinal lesions in rats--role of anti-intestinal motility mediated by D2 receptors.

BACKGROUND: Although it is known that dopamine prevents various gastrointestinal lesions, the underlying mechanism remains unclear. In the present study, we examined the protective effect of dopamine on indomethacin-induced small intestinal lesions, in relation to intestinal hypermotility. MATERIAL/METHODS: Male SD rats received indomethacin (10 mg/kg) subcutaneously (s.c.), and the small intestine was examined for lesions 24 hr later. Dopamine (1-10 mg/kg) or atropine (3 mg/kg) was administered s.c. twice, 30 min before and 8 hr after indomethacin, while sulpiride (3 mg/kg) and domperidone (3 mg/kg), the dopamine D2 receptor antagonists, or yohimbine (10 mg/kg), the alpha2-adrenoceptor antagonist, were administered s.c. twice, 30 min before each dosing of dopamine. Intestinal motility was measured using a balloon under urethane anesthesia. RESULTS: Indomethacin caused severe lesions in the small intestine, mainly both the jejunum and ileum. The intestinal ulcerogenic response to indomethacin was dose-dependently prevented by dopamine as well as atropine. The protective effect of dopamine was almost totally antagonized by domperidone and sulpiride but not by yohimbine. On the other hand, indomethacin markedly enhanced intestinal motility, and the hypermotility response was also prevented by dopamine as well as atropine. Both sulpiride and domperidone, but not yohimbine, also antagonized the inhibitory effect of dopamine on the indomethacin-induced intestinal hypermotility. CONCLUSIONS: These results suggest that dopamine protects the small intestine against indomethacin-induced damage, probably by inhibiting the intestinal hypermotility mediated by dopamine D2 receptors.

Adrenergic alpha-Antagonists↗
PubMed1993

Tissue and cell-specific patterns of expression of rat liver and intestinal fatty acid binding protein during development and in experimental colonic and small intestinal adenocarcinomas.

BACKGROUND: Mammalian small intestinal and colonic epithelium express members of a multigene family of hydrophobic ligand binding proteins of which liver and intestinal fatty acid binding protein represent among the most abundant intestinal gene products. These proteins are expressed in a cell- and region-specific manner and emerge in a temporally distinctive pattern. EXPERIMENTAL DESIGN: We have studied expression of these genes in the small intestine and colon of rats treated with 1,2-dimethylhydrazine since these animals develop a predictable pattern of both small and large bowel cancers. Studies were also undertaken in fetal and neonatal small intestine and colon. RESULTS: There was a 10- and 50-fold decrease, respectively, in mRNA abundance for intestinal and liver fatty acid binding protein in RNA from colon cancers compared with either uninvolved or control RNA. Immunocytochemical analysis revealed decreased staining for both proteins within their normal distribution together with ectopic clusters of cells reactive for liver fatty acid binding protein within colonic tumors. A more striking mosaic of immunocytochemical staining for both liver and intestinal fatty acid binding protein was found in small intestinal adenocarcinomas. Similar mosaic patterns of immunocytochemical staining were transiently detectable in rat fetal small intestine and neonatal colon. CONCLUSIONS: The region- and cell-specific expression of these genes, which may be linked temporally to events in intestinal differentiation, are subject to disruption in a cell-specific manner in the transformed, or dedifferentiated, phenotype.

1,2-Dimethylhydrazine↗
PubMed1996

Intestinal permeability and function in dogs with small intestinal bacterial overgrowth.

Small intestinal bacterial overgrowth (SIBO) has been reported to occur commonly in dogs with signs of chronic intestinal disease. There are usually few intestinal histological changes, and it is uncertain to what extent bacteria cause mucosal damage. The aim of this study was to apply a differential sugar absorption test for intestinal permeability and function to the objective assessment of intestinal damage in dogs with SIBO. Studies were performed on 63 dogs with signs of chronic small and, or, large bowel disease, in which SIBO (greater than 10(5) total or greater than 10(4) anaerobic colony forming units/ml) was diagnosed by quantitative culture of duodenal juice obtained endoscopically. None of the dogs had evidence of intestinal pathogens, parasites, systemic disease or pancreatic insufficiency. differential sugar absorption was performed by determining the ratios of urinary recoveries of lactulose/rhamnose (L/R ratio, which reflects permeability) and D-xylose/3-O-methylglucose (X/G ratio, which reflects intestinal absorptive function) following oral administration. Dogs with SIBO comprised 28 different breeds, including 13 German shepherd dogs. SIBO was aerobic in 18/63 dogs (29 per cent), and anaerobic in 45/63 (71 per cent). Histological examination of duodenal biopsies showed no abnormalities in 75 per cent, and mild to moderate lymphocytic infiltrates in 25 per cent of the dogs. The L/R ratio was increased (greater than 0.12) in 52 per cent, and the X/G ratio reduced (less than 0.60) in 33 per cent of the dogs. Differential sugar absorption was repeated in 11 dogs after their four weeks of oral antibiotic therapy. The L/R ratio declined in all 11 dogs (mean +/- SD pre: 0.24 +/- 0.14; post: 0.16 +/- 0.11; P < 0.05), but changes in the X/G ratio were more variable. These findings show that SIBO is commonly associated with mucosal damage not detected on histological examination of intestinal biopsies, and that changes in intestinal permeability following oral antibiotics may be used to monitor response to treatment.

Administration, Oral↗
PubMed1996

Longitudinal distribution of arylamine N-acetyltransferases in the intestine of the hamster, mouse, and rat. Evidence for multiplicity of N-acetyltransferases in the intestine.

Experimental and clinical evidence indicates that AcCoA:arylamine N-acetyltransferases (NATs; EC 2.3.1.5) are involved in the bioactivation and inactivation of a wide variety of arylamine, hydrazine, and carcinogenic arylamine xenobiotics. Longitudinal distribution of NATs in the intestine of the hamster, mouse, and two strains of rat was examined utilizing the model arylamine substrates procainamide(PA) and p-aminobenzoic acid (PABA) for the monomorphic (NAT1) and polymorphic (NAT2) enzymes in the rodent. NAT1 and NAT2 were distributed quite differently in each species examined. In particular, rat intestinal NATs were distributed equally throughout the intestinal tract. In contrast, hamster intestinal NATs decreased in activity from the proximal small intestine to the distal large intestine. Mouse NAT2 activity was highest in the cecum, whereas NAT1 was highest in the proximal small intestine. Although these model substrates have been shown to be selective for NATs, they are not specific. Therefore, a series of biochemical studies were undertaken to evaluate NAT multiplicity in the intestine of the F-344 rat. To assess multiplicity of NAT expression, selective inhibition, differential sensitivity to heat inactivation, and kinetic analysis were performed on intestinal cytosol. Eadie-Hofstee transformation of PA N-acetylation yielded a curvilinear plot indicative that a low affinity-high capacity enzyme aside from NAT1 (presumably NAT2) was contributing to PA N-acetylation activity. PA activity was found to exhibit approximately 4- to 5-fold greater thermostability than PABA activity. Furthermore, PA acetylation could be inhibited selectively with vinyl fluorenyl ketone (2.5 to 5 microM) but not with methotrexate (up to 2 mM). Taken together, these studies suggest the expression of both NAT1 and NAT2 in the intestine of the F-344 rat.

4-Aminobenzoic Acid↗
PubMed2003

Intestinal permeability of chlorpyrifos using the single-pass intestinal perfusion method in the rat.

The intestinal transport of chlorpyrifos (CPF), an organothiophosphate pesticide, was investigated using the single-pass intestinal perfusion (SPIP) technique in male, Sprague-Dawley rats. SPIP was performed in each isolated region of the small intestine (i.e. duodenum, jejunum and ileum) with three concentrations of CPF (0.1, 2.0 and 10 microM) at a flow rate of 0.25 ml/min. Preliminary binding and stability studies were conducted to ensure that the loss of CPF in the SPIP study can be attributed to intestinal absorption. The effective permeability (P(eff)) of CPF was determined for each segment and concentration. CPF exhibits a high intestinal permeability over the length of the small intestine indicative of compounds that are well absorbed. Decreases in permeability values at the highest CPF concentration studied in the duodenum and ileum suggest a saturable transport process. Based on these results, passive, transcellular diffusion dominates the intestinal transport mechanism of CPF, with a saturable transport process evident in the duodenum and ileum. The P(eff) of CPF is in the range of drugs with high intestinal permeability and high fraction of dose absorbed indicating that CPF readily crosses the intestine. The dependence of CPF's P(eff) on concentration in the duodenum and ileum suggests that CPF is transported by a combination of mechanisms across the intestine. Using established relationships, the human fraction dose absorbed for CPF was estimated to be >99%. The permeability values obtained from this study may be useful in models of exposure assessment.

Algorithms↗
PubMed1983

Characterization of human foetal intestinal alkaline phosphatase. Comparison with the isoenzymes from the adult intestine and human tumour cell lines.

The molecular structure of human foetal intestinal alkaline phosphatase was defined by high-resolution two-dimensional polyacrylamide-gel electrophoresis and amino acid inhibition studies. Comparison was made with the adult form of intestinal alkaline phosphatase, as well as with alkaline phosphatases isolated from cultured foetal amnion cells (FL) and a human tumour cell line (KB). Two non-identical subunits were isolated from the foetal intestinal isoenzyme, one having same molecular weight and isoelectric point as placental alkaline phosphatase, and the other corresponding to a glycosylated subunit of the adult intestinal enzyme. The FL-cell and KB-cell alkaline phosphatases were also found to contain two subunits similar to those of the foetal intestinal isoenzyme. Characterization of neuraminidase digests of the non-placental subunit showed it to be indistinguishable from the subunits of the adult intestinal isoenzyme. This implies that no new phosphatase structural gene is involved in the transition from the expression of foetal to adult intestinal alkaline phosphatase, but that the molecular changes involve suppression of the placental subunit and loss of neuraminic acid from the non-placental subunit. Enzyme-inhibition studies demonstrated an intermediate response to the inhibitors tested for the foetal intestinal, FL-cell and KB-cell isoenzymes when compared with the placental, adult intestinal and liver forms. This result is consistent with the mixed-subunit structure observed for the former set of isoenzymes. In summary, this study has defined the molecular subunit structure of the foetal intestinal form of alkaline phosphatase and has demonstrated its expression in a human tumour cell line.

Alkaline Phosphatase↗
PubMed2005

Morphology of myenteric plexuses in the human large intestine: comparison between large intestines with and without colonic diverticula.

BACKGROUND: Large intestines with diverticula exhibit functionally abnormal peristaltic activity and elevated luminal pressure that may indicate functional changes in the myenteric plexus; however, no studies have investigated the characteristics of either normal or diverticula myenteric plexuses. METHODS: Tissue specimens obtained from 93 colorectal cancer patients without diverticula, 14 patients with perforated diverticulitis, and 12 colorectal cancer patients with asymptomatic diverticula were included in this study. Myenteric plexuses and ganglion cells were counted per centimeter, and the area and maximum diameter of the nuclei of ganglion cells were measured using an image analyzer. RESULTS: The number of myenteric plexuses and ganglion cells per centimeter was significantly higher in the descending colon, sigmoid colon, and rectum than in the cecum, ascending colon, and transverse colon. The area of the nuclei of ganglion cells was significantly larger in the descending colon and sigmoid colon than in the cecum and ascending colon. Compared with large intestines without diverticula, the number of myenteric plexuses was significantly higher in large intestines with diverticula, whereas the number of ganglion cells decreased in both right-sided and left-sided large intestines with perforated diverticulitis or asymptomatic diverticula. The area of the nuclei of ganglion cells was significantly smaller in large intestines with diverticula. CONCLUSION: The morphology of myenteric plexuses and the ganglion cells differs significantly among segments of the human large intestine. Large intestines with diverticula had significantly more plexuses but significantly fewer ganglion cells than large intestines without diverticula. The area of the nuclei of ganglion cells was also significantly smaller in large intestines with diverticula. Further studies are required to clarify how these changes are related to intestinal function and how they are involved in the etiology of diverticulosis.

Adult↗
PubMed1992

An intestinal galactose-specific lectin mediates the binding of murine IgE to mouse intestinal epithelial cells.

A number of lactose-binding lectins have recently been identified in the rat and mouse intestine, one of which corresponds to the C-terminal domain of IgE-binding proteins, originally identified in rat basophilic leukemia (RBL) cells and mouse 3T3 fibroblasts. In the present report, we describe the affinity purification of a rat intestinal lactose-specific lectin which binds murine IgE antibodies. This binding most likely occurs via the immunoglobulin carbohydrate chains, as it is inhibited by lactose. This intestinal lectin molecule is also immunologically related to the previously described IgE-binding protein (epsilon BP) isolated from RBL cells, since it is recognized by antibodies raised against recombinant epsilon BP. This intestinal form of epsilon BP has a molecular mass of 17.5 kDa, which is much lower than that of its RBL cell analogue (31 kDa). The attachment of IgE to the mouse intestinal epithelium was demonstrated by immunohistochemistry, along with the presence of a corresponding mouse intestinal epsilon BP. The carbohydrate-dependent nature of this attachment was established by demonstrating that IgE binding to mouse epithelium was specifically abolished by lactose (4 mM) and by a blood-group-A-active tetrasaccharide (0.2 mM), but not by mannose (10 mM). Finally, the association of IgE with the mouse intestinal epithelium was prevented by competition with the purified IgE-binding lectin isolated from rat intestine. Although the physiological function of this intestinal protein is still unknown, the finding that IgE binds to a lectin in the intestinal epithelium pinpoints a possible novel mechanism for the regulation of IgE-mediated disorders, such as food allergy.

3T3 Cells↗
PubMed1994

Increased intestinal marker absorption due to regional permeability changes and decreased intestinal transit during sepsis in the rat.

BACKGROUND: The intestinal barrier properties are impaired during inflammation and sepsis, but the mechanisms behind this are unknown and were therefore investigated during experimental sepsis in rats. METHODS: The different-sized intestinal absorption markers 51Cr-labeled ethylenediaminetetraacetic acid (EDTA) and ovalbumin were gavaged to rats made septic by intra-abdominal bacterial implantation and to sham-operated rats. Regional tissue permeability was measured in diffusion chambers, and intestinal transit was evaluated by intestinal accumulation of gavaged 51Cr-EDTA. RESULTS: In comparison with the sham-operated rats, septic rats had higher 51Cr-EDTA levels in blood and urine and showed a prolonged intestinal transit. Septic rats also had a lower tissue permeability to both markers in the small intestines but higher permeability to ovalbumin in the colon. Rats receiving morphine to decrease intestinal motility showed similar changes, with a decreased intestinal transit and increased marker absorption. CONCLUSIONS: The results suggest that the increased intestinal absorption during sepsis was due to regional permeability changes and prolonged intestinal transit.

Animals↗