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PubMed1976

[Adaptive changes in intestinal mucosa of the small intestine as a result of intraluminal stress].

Under physiological conditions, the intestinal mucosa is the site of a delicate balance between cell proliferation in the crypt region and cell desquamation at the villus tips. This balance can be deranged by a number of endogenous or exogenous factors, oneof which is the intraluminal contents. This review discusses the effects of different modifications of the luminal milieu on the structure and function of the mucosa. Following intestinal resection or loop transposition, the contents reaching the remnant or the transposed loop differ markedly from those with which they come into contact under normal conditions. Hyperplasia without zonal transformation then develops in the experimental loop. The villi do not become wider, and changes in the strucutre of the epithelium are not observed. There are conflicting resutls in the literature concerning the enzyme activities in the individual enterocytes resulting from this hyperplasia. However, the epithelium its functionally immature, since transport capacities measured in vitro are reduced. On the other hand, the hyperplasia of the mucosa is such that absorptive capacities in vivo, when expressed in terms of intestinal length, are larger than normal. When the intestine is subjected to prolonged infusion of lactic acid, the enterocytes are damaged and increased exfoliation results. A similar result is obtained in the blind-loop syndrome, where the accumulation of bile acids and bacteria provides the stress responsible for the destruction of the enterocytes, and in non-tropical spure, where the epithelium is attacked by noxious peptides in the diet. The first consequence of the accelerated desquamation is epithelial hyperplasia without zonal transformation, though the enterocytes are damaged - in contrast to those of the resected intestine - and apparently possess reduced enzyme activities. If the application of the stress is continued, a stage is reached in which the cell proliferation does not suffice to counteract the cell loss at the villus tips. Then a zonal transformation occurs whereby, despite the lengthened crypts, the villi become shorter and wider until, in extreme cases, the mucosa is completely devoid of villi. The transport capacity in vitro and in vivo - even when expressed in terms of unit-length is reduced, and good correlations exist between the reduction in function and the diminution in surface area of the intestine. In a self-emptying blind loop, the intestine is devoid of all contact with nutritional material. Under these circumstances, hypoplasia of the mucosa develops in which the enterocytes appear unchanged, though in extreme cases they may possess reduced enzyme levels, and the absorption capacity in vivo is consequently reduced.

Adaptation, Physiological↗

PubMed1990

Enhanced intestinal permeability to 51Cr-labeled EDTA in dogs with small intestinal disease.

Intestinal permeability in dogs with small intestinal disease was measured by quantitation of 24-hour urinary excretion of 51Cr-labeled EDTA following intragastric administration. Permeability was high in dogs with a variety of naturally acquired small intestinal diseases including wheat-sensitive enteropathy of Irish Setters, small intestinal bacterial over-growth, and giardiasis, and permeability was decreased after successful treatment. These findings indicate that the assessment of intestinal permeability may be a useful technique for detecting small intestinal disease and for monitoring the efficacy of treatment in dogs.

Animals↗

PubMed2001

Identification of Paneth cells in pyloric glands associated with gastric and intestinal mixed-type intestinal metaplasia of the human stomach.

We have proposed that intestinal metaplasia (IM) of the human stomach be divided into two types on the basis of cell differentiation status: a gastric and intestinal (GI) mixed type and a solely intestinal (I) type. In the GI mixed type, gastric (foveolar epithelial and pyloric gland cells) and intestinal (goblet, intestinal absorptive, and Paneth cells) phenotype cells coexist in the same intestinalized gastric glands in various combinations and degrees. Consequently, intestinalized gastric glands are hybrids. Although we have described the rare appearance of Paneth-like cells in pyloric glands of GI mixed-type IM, the absence of an appropriate Paneth cell marker leaves room for doubt as to their true character. The purpose of this study was to clearly identify Paneth cells in pyloric glands in IM lesions using a new Paneth cell marker, a polyclonal antibody human defensin (HD)-5, raised against HD-5, which is included in granules of Paneth cells. A total of 105 gastric samples (4 biopsy and 101 surgical resected specimens) were examined. In only nine cases (8.6%), the antibody allowed demonstration of Paneth cells in pyloric glands in GI mixed-type IM, confirming our previous finding. Analysis of the proliferative cell (P) zone indicated that a common stem cell might generate both GI phenotype cells by upward and downward migration. No Paneth cells were found above the P zone. The results suggest that the stem cells show abnormal cell differentiation in IM lesions but preserve their normal direction of migration.

Adenocarcinoma↗

PubMed1987

Effect of bromelain on alkaline phosphatases of intestinal and non-intestinal tissues and serum.

Human alkaline phosphatases extracted with butanol from liver, kidney and placenta, and from foetal and adult small intestine each contain fragments with molecular masses within the range of approximately 8 kDa to 20 kDa which can be removed by digestion with bromelain. However, in the case of adult intestine, this fragment (which is presumed to represent a membrane-binding domain) can only be demonstrated in tissue extracted immediately after removal at operation. Similar fragments are also present in foetal intestinal phosphatase in amniotic fluid, and in liver and bone alkaline phosphatases recovered from serum. Again, however, adult intestinal phosphatase from serum differs in the absence of the bromelain-sensitive fragment. These observations indicate differences in the ways in which intestinal and non-intestinal alkaline phosphatases gain access to the circulation, and also have implications for structural studies on intestinal phosphatase extracted post mortem from adult tissue.

Adult↗

PubMed1985

Study of intestinal cell differentiation with monoclonal antibodies to intestinal cell surface components.

Monoclonal antibodies that react with antigens of the plasma membrane of rat intestinal villus and crypt cells have been prepared by fusion of mouse myeloma (NSI) cells with spleen cells of mice immunized with various intestinal cellular fractions, including the luminal membrane of adult villus and crypt cells, and of newborn rat intestinal cells. The antigenic targets of most antibodies have been identified. They include major protein components of the brush border (luminal) membrane of adult villus cells (sucrase-isomaltase, maltase, lactase, aminopeptidase N, alkaline phosphatase) and newly identified protein antigens specific for intestinal epithelial cells. Of 25 independently derived monoclonal antibodies prepared, 18 reacted exclusively with the brush border membrane of the villus cells, confirming its unique protein composition. Antibodies specifically staining the crypt cells, the newly differentiated epithelial cells present in the lower half of the villi, the top villus cells, and both villus and crypt cells were also obtained and characterized. These antibodies have been used to study the expression of cell- and tissue-specific functions during differentiation and development of the intestinal epithelium. Contrary to results obtained with polyclonal antisera, no inactive forms of the brush border enzymes have been detected in the crypt cells. The identification of cell surface components expressed at different levels of the villi, and in both undifferentiated and differentiated intestinal cells, suggests that cell differentiation in the intestinal epithelium is a continuous and gradual process involving both transcriptional and translational regulation of different sets of genes.

Alkaline Phosphatase↗

PubMed1996

Effects of the intestinal flagellate, Cochlosoma anatis, on intestinal mucosal morphology and disaccharidase activity in Muscovy ducklings.

Newly hatched female Muscovy ducklings were randomly separated into 2 groups of 12 and 1 group of 13. Ducklings in the first 2 groups were each orally inoculated with 0.5 ml of sterile normal saline containing 0 and 3 x 10(6) trophozoites of Cochlosoma anatis, respectively. Birds in the third group were each orally inoculated with 3 x 10(6) trophozoites for 5 consecutive days. Birds were weighed daily for the first 5 days and then on days 7, 14 and 21 post-inoculation (p.i.). On days 6, 7, 8, 13, 14, 15, 20, 21 and 22 p.i., 1 bird from each group was killed and samples of intestine at 7 levels were taken for trophozoite counts, mucosal disaccharidase analyses and morphometric analysis. Body weights did not differ among treatment groups at any time during the experiment. Trophozoite numbers did not change over the period 6-22 days p.i. Trophozoite numbers were lowest in the anterior small intestine and increased distally, but very few were observed in the caecum. Crypt depth was greater in all regions of the small intestine in inoculated groups compared to uninoculated controls, and was significantly increased in the duodenum, proximal jejunum and mid-jejunum (P < 0.05). Villus height was greater in inoculated groups compared to controls at all levels of the intestine and was significantly increased in the duodenum, proximal jejunum and ileum (P < 0.05). Mucosal palatinase and maltase activity in the small intestine were reduced in inoculated groups compared to uninoculated controls; palatinase activities were significantly reduced in the proximal and mid-jejunum and maltase activities were significantly reduced in the mid-jejunum (P < 0.05). Sucrase activities were significantly increased at all levels of the small intestine in inoculated ducklings compared to uninoculated controls (P < 0.05). Although no clinical signs were evident, Cochlosoma infection significantly altered intestinal morphometrics and mucosal enzyme concentrations in ducklings, in several cases in a counter-intuitive direction.

Animals↗

PubMedDate not supplied

Temporary elevation of serum transaminases after pediatric intestinal transplantation: incidence and clinical correlation in multivisceral transplant vs isolated intestinal transplant.

Data were gathered from the records of 51 children of median age 1.5 years who survived more than 6 months after intestinal transplantation. Abnormal liver function tests (LFTs) were defined as serum aspartate aminotransferase (AST) greater than 100 IU/L or total bilirubin greater than 2.0 g/dL lasting more than 3 days. Temporary elevation was defined when LFTs returned to normal without graft loss or death. LFT elevation at the time of transplantation was not included as a temporary LFT elevation. Median follow-up was 36 months. In multivisceral transplant recipients, all patients (n = 34) showed abnormal LFTs at transplantation that normalized within a median period of 2 days. Temporary LFT elevations were seen in 20 of 34 (59%) in multivisceral transplantation and 5 of 17 (29%) in isolated intestinal transplantation. Median length of elevation was 14 days in multivisceral transplantation and 12 days in isolated intestinal transplantation. Peak AST was 353 +/- 190 IU/dL in multivisceral transplantation and 839 +/- 605 IU/dL in isolated intestinal transplantation (P = .0059). Events associated with temporary LFT elevations in multivisceral transplantation were total parental nutrition (TPN) (n = 8), dehydration (n = 2), viral infection (n = 2), others (n = 3), and nonspecific (n = 5). Events in isolated intestinal transplantation were posttransplant lymphoproliferative disorder (n = 2), TPN (n = 1), and nonspecific (n = 2). Temporary LFT elevations were commonly seen among pediatric intestinal recipients, which correlated with events other than rejection. Approximately half of the temporary LFT elevations were associated with no significant clinical events. They resolved spontaneously. Interestingly, the peak AST value was higher in isolated intestinal transplantation compared to multivisceral transplantation.

Adolescent↗

PubMed1999

Experimental small bowel transplantation using newborn intestine in rats: II. Revascularization of newborn intestine is independent of vascular endothelial growth factor.

BACKGROUND: Fetal and newborn intestine often are revascularized after subcutaneous transplantation without surgical vascular anastomosis. However, the mechanism of this ability remains unclear. METHODS: First, the ability of natural revascularization in newborn organs was tested. Newborn organs in whole (liver, kidney, heart, intestine, spleen, and pancreas) were grafted i nto the subcuta neous tissue of the adult rat and evaluated histopathologically 2 weeks after transplantation. Second, expression of vascular endothelial growth factor (VEGF) mRNA in the intestinal graft was determined before and after transplantation. Finally, we tested whether the free graft survival of newborn intestine was interrupted by TNP-470, an antiangiogenic agent. RESULTS: Spleen and intestine were revascularized at a higher rate (91.6%, 75%, respectively), and kidney and heart grafts survived at a lower rate (41.7%, 25%, respectively). But all of liver and pancreas grafts failed to be revascularized. VEGF mRNA was not induced in the course of revascularizing. Furthermore, TNP-470 did not interfere with neovascularization of the newborn intestinal graft in vivo. CONCLUSIONS: Each organ had an organ-specific angiogenic activity. Neovascularization of intestinal graft was not dependent on VEGF expression.

Angiogenesis Inhibitors↗

PubMedDate not supplied

Intestinal flora and nutrient absorption after intestinal resection.

Intestinal resection results in loss of surface area, motor disruption, and an altered luminal milieu, all of which might influence bacterial growth. Our aim was to determine the effect of extensive intestinal resection in the dog on small intestinal bacterial flora and nutrient absorption. Ten dogs underwent 75% proximal intestinal resection and were killed at either 12 or 40 weeks. Five animals underwent transection alone and were killed at 12 weeks. Ileal aspirates were cultured. Nutritional status and nutrient absorption were measured every 4 weeks. Mean total and anaerobic ileal flora were increased after resection, significantly at 40 weeks. Overall, more cultures from resected animals had more than 5x10(6) total bacteria (6 of 10 vs. 0 of 10, P<0.05) and more than 10(5) anaerobic bacteria (5 of 10 vs. 0 of 10, P<0.05) than unoperated animals. Total but not anaerobic bacteria were increased after transection alone. Ingestion and absorption of carbohydrate decreased but absorption efficiency was maintained. Nitrogen intake decreased but excretion and absorption were unchanged. Fat intake decreased and excretion was unchanged resulting in decreased absorption. Mean intake, excretion, and absorption of nutrients were not influenced by the presence of significant growths of total (>5x10(6)/ml) or anaerobic (>10(5)/ml) bacteria. It was concluded that (1) 75% proximal intestinal resection results in significantly more aerobic and anaerobic bacteria in the ileal remnant; (2) intestinal bacterial content does not correlate with absorption of nutrients; and (3) the colon, and particularly colonic bacteria, may have a more important role in nutrient absorption than luminal flora in the small intestine after resection.

Absorption↗

PubMed2004

Validation of intramural intestinal microdialysis as a detector of intestinal ischaemia.

BACKGROUND: The purpose of this study was to validate intestinal microdialysis as a detector of intestinal ischaemia using measurements of glucose, lactate and glycerol from the jejunal wall. METHODS: Based on a previous study, the cut-off levels for the presence of regional intestinal ischaemia were defined for microdialysis glucose, lactate, glycerol and the lactate/glucose ratio. Changes of 60% in the metabolic compounds measured after 100 min were defined as the cut-off level for ischaemia. The cut-off levels were tested in a randomized, single-blinded study. Ten pigs were used; occlusive ischaemia was performed by clamping a segment of the mesentery to the intestine. Four catheters were inserted per pig, two in the ischaemic segment and two in the non-ischaemic segment. All catheters were numbered, randomly allocated and inserted in the intestine by the staff at the institute and unknown to the investigators. RESULTS: One pig was excluded because the clamping was insufficient. Technical problems with the catheters were registered in 15% of cases owing to damage of the microdialysis membrane, dislocation, or incorrect placement. The predictive values of presence of ischaemia for glucose, lactate, glycerol and the lactate/glucose ratio were: 0.91, 1,0.85 and 0.92, respectively. CONCLUSION: Using a 60% cut-off limit measured after 100 min, intestinal ischaemia can be detected and excluded using intestinal microdialysis, but some technical problems remain that need further investigation.

Animals↗

PubMed1999

Neonatal exposure to the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine via breast milk or directly induces intestinal tumors in multiple intestinal neoplasia mice.

We examined whether the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) could increase intestinal tumorigenesis in neonatal C57BL/6J-Min/+ mice, a murine model for familial adenomatous polyposis. Min/+ mice are heterozygous for a nonsense mutation in the adenomatous polyposis coli gene and spontaneously develop multiple intestinal adenomas, primarily in the small intestine. Neonatal Min/+ mice (3-6 days old) were exposed to PhIP via breast milk from lactating dams given 8 s.c. injections of 50 mg/kg PhIP three times a week or to 8 s.c. injections of 25 or 50 mg/kg PhIP directly, over the same period. At the age of 11 weeks, the number, diameter and location of the intestinal tumors were scored. Remarkably, a 2- to 4-fold increase in the number of small intestinal tumors was seen in Min/+ mice exposed to PhIP via breast milk (P < 0.001). To our knowledge, this is the first time PhIP has been reported to induce tumors following exposure via breast milk from PhIP-exposed dams. Upon direct exposure to 50 mg/kg PhIP, a 6- to 9-fold increase in the number of small intestinal tumors was observed (P < 0.001). The diameter of the PhIP-induced small intestinal tumors was slightly increased (P < 0.001). In the colon, a 3- to 4-fold increase in the number of tumors was seen in Min/+ mice exposed to PhIP via breast milk (P = 0. 004). Direct exposure to 50 mg/kg PhIP caused a 2- to 6-fold increase in the number of colonic tumors (P = 0.014). The PhIP-induced colonic tumors were located more distally and displayed a smaller diameter than the tumors from the controls (P < 0.05). In contrast to a previous study, where PhIP showed only a moderate tumorigenic effect in adult Min/+ mice, the present study demonstrates a strong tumorigenic effect of PhIP in neonatally exposed Min/+ mice, even after exposure via breast milk from PhIP-exposed dams.

Animals↗

PubMed2002

The food mutagen 2-amino-9H-pyrido[2,3-b]indole (AalphaC) but not its methylated form (MeAalphaC) increases intestinal tumorigenesis in neonatally exposed multiple intestinal neoplasia mice.

The heterocyclic amines 2-amino-9H-pyrido[2,3-b]indole (AalphaC) and 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeAalphaC) are carcinogenic in several organs in rodents, but not in the intestinal tract. However, AalphaC induces DNA adducts, mutations and preneoplastic aberrant crypt foci (ACF) in rodent colons. The purpose of this study was to examine whether AalphaC and MeAalphaC could affect intestinal tumorigenesis in C57BL/6J-Min/+ (multiple intestinal neoplasia) mice. These mice are heterozygous for a germline nonsense mutation in codon 850 of the tumor suppressor gene adenomatous polyposis coli (Apc), producing a truncated non-functional Apc protein. They develop multiple intestinal adenomas, and are particularly susceptible to intestinal carcinogens that affect the Apc gene, especially when exposed neonatally. Whole litters consisting of Min/+ and +/+ (wild-type) mice of both sexes were given a single s.c. injection of 0.22 mmol/kg AalphaC (40.3 mg/kg) or MeAalphaC (43.4 mg/kg) or the vehicle 1:1 dimethylsulfoxide:0.9% NaCl on days 3-6 after birth, and were terminated at 11 weeks. AalphaC increased the number and diameter of small intestinal tumors, but not the number of colonic tumors or dysplastic ACF, in female and male Min/+ mice separately. In pooled data from females and males, colonic tumors and ACF found after AalphaC exposure appeared to be smaller than the spontaneous lesions, indicating later induction, slower growth or both. In contrast to AalphaC, MeAalphaC did not affect intestinal tumorigenesis in Min/+ mice. No effects were found by any of the amino-alpha-carbolines in the +/+ mice. AalphaC was less potent than the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.

Animals↗

PubMed1998

Vitamin A up-regulates expression of bone-type alkaline phosphatase in rat small intestinal crypt cell line and fetal rat small intestine.

Vitamin A is a potent inducer for liver/bone/kidney alkaline phosphatase (L/B/K ALP) in a variety of tissues. However, the evidence for induction of L/B/K ALP by vitamin A in small intestine is limited. In this study, we investigated the influence of vitamin A on L/B/K ALP expression in rat small intestinal crypt IEC-6 cells and fetal rat small intestine. Treatment of IEC-6 cells with all-trans retinoic acid (RA) increased the levels of activity, protein and mRNA of L/B/K ALP, whereas enterocyte-specific proteins, including intestinal ALP, sucrase-isomaltase and glucose transporter-2, were not induced. The reverse transcription-polymerase chain reaction technique revealed that this L/B/K ALP transcript had the bone-type but not the liver-type leader exon. IEC-6 cells constitutively expressed mRNAs of all subtypes of retinoic acid receptor (RAR) and retinoid X receptor (RXR) at varied concentrations. Among these receptor mRNAs, RARbeta mRNA quickly responded to RA treatment, and the level was doubled within 4 h. Gel mobility shift assay showed that RA induced an RXRE-binding activity in IEC-6 cells. The L/B/K ALP transcript, expressed in fetal rat small intestine, also contained the bone-type leader exon. Intragastric administration of 10 mg retinyl acetate to pregnant rats from gestational d 7 to 15 increased the levels of this transcript and enzyme in 15-d fetal rat small intestine. Our results suggest that vitamin A may be an important regulator for L/B/K ALP expression in fetal rat small intestine as well as in IEC-6 cells.

Alkaline Phosphatase↗

PubMed2005

Short-chain fatty acid induces intestinal mucosal injury in newborn rats and down-regulates intestinal trefoil factor gene expression in vivo and in vitro.

BACKGROUND: Luminal administration of short-chain fatty acids (SCFAs) induces dose-dependent intestinal mucosal injury in newborn rats. However, the mechanism underlying the injurious effects of SCFAs on intestinal mucosa in neonates is unclear. Intestinal trefoil factor (ITF) is a factor important for the maintenance and repair of the intestinal mucosal barrier. Regulation of ITF gene expression by SCFAs may be involved as one of the mechanisms. OBJECTIVES: To examine the effect of butyrate-induced colonic injury on ITF gene expression in vivo and to determine the molecular mechanisms underlying the butyrate regulation of ITF gene expression in vitro. METHODS: Whole-section colonic tissues from 9- to 10-day-old Sprague-Dawley rats that have received butyric acid at two different concentrations (150 mmol/L and 300 mmol/L) and for different time periods were processed for total RNA extraction and Northern blot analysis. Littermates that received normal saline or lactic acid at 300 mmol/L served as controls. The effect of butyrate on ITF gene expression was also examined in vitro with human colonic epithelial LS 174T cells. To further define ITF gene regulation by butyrate, transient transfection assays were performed on a 930 bp human ITF promoter-luciferase reporter gene plasmid in LS174T cells with or without the presence of butyrate. RESULTS: Concurrent with mucosal injury, butyric acid inhibited ITF gene expression in colonic tissues of newborn rats as well as in intestinal epithelial cells in a dose- and time-dependent manner. Furthermore, butyrate reduced ITF promoter report gene activity in transfected LS174T cell, suggesting that butyric acid regulation of ITF gene is by way of a specific ITF promoter. CONCLUSIONS: Butyric acid induced-intestinal mucosal injury in newborn rats is associated with down-regulation of ITF gene expression. The changes in ITF gene expression in vivo may play a role in the pathogenesis of SCFA-induced intestinal mucosal injury.

Animals↗

PubMed1994

Rotavirus-specific intestinal immune response in mice assessed by enzyme-linked immunospot assay and intestinal fragment culture.

Primate rotavirus strain RRV and bovine strain WC3 or reassortants made between these animal viruses and human rotaviruses have been administered to infants as candidate vaccines. We compared RRV and WC3 in a murine model of oral infection. We determined the relative capacities of these viruses to induce a virus-specific humoral immune response by intestinal lymphocytes as tested by enzyme-linked immunospot assay, intestinal fragment culture, and enzyme-linked immunosorbent assay of intestinal contents. We found that inoculation of mice with RRV induced higher frequencies of virus-specific immunoglobulin A (IgA)-secreting cells in the lamina propria, greater quantities of virus-specific IgA in intestinal fragment cultures, and greater quantities of virus-specific IgA in intestinal secretions than did inoculation with WC3 or inactivated RRV (iRRV). The induction of an IgA response in serum was predictive of an IgA response among intestinal lymphocytes after inoculation with RRV but not WC3. In addition, large quantities of IgG, IgA, and IgM not specific for rotavirus were produced in fragment cultures from mice inoculated with RRV but not in cultures from mice inoculated with WC3 or iRRV. Possible mechanisms of RRV-induced polyclonal stimulation of intestinal B cells are discussed.

Animals↗

PubMed1988

Roles of motility, chemotaxis, and penetration through and growth in intestinal mucus in the ability of an avirulent strain of Salmonella typhimurium to colonize the large intestine of streptomycin-treated mice.

Previously, it had been shown that an avirulent strain of Salmonella typhimurium, SL5316, with wild-type lipopolysaccharide (LPS) was a far better colonizer of the streptomycin-treated CD-1 mouse large intestine, was far more motile, did not bind to mouse intestinal mucus nearly as well as, but penetrated through a layer of intestinal mucus in vitro far better than an almost isogenic LPS-deficient transductant, SL5325. In the present investigation, a nonflagellated transductant, SL5681, and a nonchemotactic transductant, SL5784, were isolated from SL5316 and tested for relative colonizing ability versus SL5316 (smooth) and SL5325 (rough) in streptomycin-treated mice. In addition, the Salmonella strains were tested for their ability to grow together in cecal intestinal mucus and in cecal luminal contents, for their tumbling and swimming activities after growth in cecal mucus, and for their ability to adhere to and travel through cecal mucus in vitro. The data show that the nonflagellated and nonchemotactic derivatives colonized large intestine nearly as well as their parent and were far better colonizers than the LPS-deficient mutant, that all the strains grew equally well in cecal mucus but did not grow in cecal luminal contents, and that cecal mucus-grown strains lost tumbling and swimming activities. Furthermore, the LPS-deficient strain adhered to cecal mucus far better but penetrated mucus far worse than did the nonflagellated transductant, the nonchemotactic transductant, and the parent. Thus, motility and chemotaxis do not appear to play a major role in the ability of the avirulent S. typhimurium strains to colonize the mouse large intestine, colonization may require growth in cecal mucus but does not depend on growth in cecal luminal contents, growth in cecal mucus inhibits S. typhimurium motility, and increased adhesion of the LPS-deficient mutant to cecal mucus and its poor ability to penetrate cecal mucus may play a role in its poor intestine-colonizing ability.

Animals↗

PubMed1989

Viability of the vascularly perfused, recirculating rat intestine and intestine-liver preparations.

Function and stability of vascularly perfused, recirculating in situ rat intestine (I) and intestine-liver (IL) preparations were evaluated in fasted and nonfasted rats because these techniques may be readily applied in drug metabolism studies. The rat intestine was perfused with blood medium (7.5 ml/min) via the superior mesenteric artery, with the venous outflow draining into the portal vein, which, together with hepatic arterial flow (2.5 ml/min), constituted the total blood flow (10 ml/min) to the liver. Maintenance of intestinal membrane integrity was observed. Rapid [14C]glucose absorption against a concentration gradient and a lack of [3H]-polyethylene glycol 4000 (PEG 4000, less than 4%) and Evans blue absorption by the recirculating I and IL preparations resulted after bolus injections of these markers into the pyloric end of the duodenum. Other indexes that revealed stable intestinal and liver functions were the following: preservation of reservoir perfusate volume, constancy in perfusion pressure, bile flow, and hemoglobin concentrations, evidence of intestinal glucose utilization and liver glucose production, and a lack of significant leakage of serum glutamic oxalic transaminase. The intestine and liver consumed oxygen at relatively constant rates, but the consumption rates for the fasted tissues (I or L) were significantly higher than those for nonfasted tissues. These results indicate that the vascularly perfused I and IL preparations were maintained in a viable and stable state for a 2-h perfusion period.

Animals↗

PubMed2005

Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy.

Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum (n = 8) or infant formula (n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed (n = 8) or fed colostrum (n = 7) or formula (n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.

Animals↗