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Peripheral engraftment of fetal intestine into athymic mice sponsors T cell development: direct evidence for thymopoietic function of murine small intestine.

Adult athymic, lethally irradiated, F1-->parent bone marrow-reconstituted (AT x BM) mice were engrafted bilaterally with day 16-18 fetal intestine or fetal thymus into the kidney capsule and were studied for evidence of peripheral T cell repopulation of 1-12 wk postengraftment. Throughout that time period, both types of grafts were macroscopically and histologically characteristic of differentiated thymus or intestine tissues, respectively. Beginning at week 2 postengraftment, clusters of lymphocytes were present within intestine grafts, particularly in subepithelial regions and in areas below villus crypts. As determined by immunofluorescence staining and flow cytometric analyses, lymphocytes from spleen and lymph nodes of sham-engrafted mice (AT x BM-SHAM) were essentially void of T cells, whereas in AT x BM thymus-engrafted (AT x BM-THG) mice, which served as a positive control for T cell repopulation, normal levels of T cells were present in spleen and lymph nodes by week 3 postengraftment, and at times thereafter. Most striking, however, was the finding that T cell repopulation of the spleen and lymph nodes occurred in AT x BM fetal intestine-engrafted (AT x BM-FIG) mice beginning 3 wk postengraftment. Based on H-2 expression, peripheral T cells in AT x BM-FIG mice were of donor bone marrow origin, and consisted of CD3+, T cell receptor (TCR)-alpha/beta+ T cells with both CD4+8- and CD4-8+ subsets. Peripheral T cells in AT x BM-FIG mice were functionally mature, as demonstrated by their capacity to proliferate after stimulation of CD3 epsilon. Moreover, alloreactive cytotoxic T lymphocytes were generated in primary in vitro cultures of spleen cells from AT x BM-FIG and AT x BM-THG mice, though not in spleen cell cultures from AT x BM-SHAM mice. Histologic studies of engrafted tissues 3-4 wk postengraftment demonstrated that thymus leukemia (Tl) antigens were expressed on epithelial surfaces of intestine grafts, and that both TCR-alpha/beta+ and TCR-gamma/delta+ lymphocytes were present in intestine grafts. Collectively, these findings indicate that the murine small intestine has the capacity to initiate and regulate T cell development from bone marrow precursors, thus providing a mechanism by which extrathymic development of intestine lymphocytes occur.

Animals↗

Resuscitation-induced intestinal edema decreases the stiffness and residual stress of the intestine.

We have shown that acute edema impairs intestinal transit and we wanted to know whether this could be from changes in the physical characteristics of the intestine. Our hypothesis was that acute edema will change the physical characteristics of the intestine, which were measured by standardized engineering measures of elastic modulus, to determine stiffness and opening angle, and to determine residual stress. Rats were randomized to sham, mild edema (80 mL/ kg of normal saline resuscitation), and severe edema groups (80 mL/kg of normal saline resuscitation with intestinal venous hypertension). Segments of distal ileum were hung to a fixed point in a tissue bath and to a tensiometer and were stretched in increments of 1 mm, recording the new length and the corresponding force from the tensiometer to determine elastic modulus. Next, two transverse cuts were made yielding a 1- to 2-mm-thick ring-shaped segment of tissue and were then cut radially to open the ring. The opening angle was measured. Acute intestinal edema led to a decrease in transit, elastic modulus, and opening angle of the intestine in the absence of ischemic injury. Acute intestinal edema leads to a significant loss in stiffness and residual stress and is a plausible explanation for how acute edema impairs intestinal transit.

Animals↗

Intestinal mesenchyme provokes differentiation of intestinal endocrine cells in gizzard endoderm.

The gizzard (muscular stomach) of chicks is deficient in endocrine cells at hatching. It has previously been shown that proventricular types and proportions of endocrine cells can be induced in gizzard endoderm under the influence of proventricular (glandular stomach) mesenchyme. In order to test its capacity to form nongastric endocrine cell types, gizzard endoderm of 3.75- to 5-day chick embryos was combined with mesenchyme from the small intestine of 3.5- to 4-day quail embryos. The combinations were grown as chorio-allantoic grafts until they attained an incubation age comparable to that of hatching chicks. Controls comprised reassociated endoderm and mesenchyme of chick gizzard and of quail intestine. In the experimental grafts, morphogenesis was predominantly intestinal but some grafts showed gizzard-like features, particularly if the endoderm had been provided by older donors. All intestinal endocrine cell types, including those also found in the normal proventriculus (serotonin-, glucagon-, pancreatic polypeptide-, neurotensin- and somatostatin-immunoreactive cells) differentiated in experimental grafts, some even where morphogenesis was gizzard-like. Hence progenitors of not only gastric, but also intestinal, endocrine cells are indeed present in gizzard endoderm. The possibility that gizzard mesenchyme is inhibitory to endocrine cell differentiation is mooted. Motilin- and secretin-immunoreactive cells, which are characteristic of the intestine but not of the proventriculus of chicks at hatching, were respectively sparse or absent when the endoderm was derived from older donors. Thus the ability of gizzard endoderm to differentiate into nongastric endocrine cell types declines before its capacity to form gastric types. The unexpected appearance of gastrin-releasing peptide (GRP)-immunoreactive cells, a proventricular type not found in normal chick intestine, suggests that the intestinal mesenchyme, at least in this instance, was exercising a permissive role.

Animals↗

Inhibitory mechanism of intestinal ethanol absorption induced by high acetaldehyde concentrations: effect of intestinal blood flow and substance specificity.

This study describes the effects of high blood acetaldehyde concentrations on the intestinal absorption of ethanol and 2-butanone using an in situ single-pass perfusion technique on the rat intestine and the colored microsphere method to measure intestinal blood flow. We found that high blood acetaldehyde concentrations inhibit intestinal ethanol absorption in an inverse proportion to peak acetaldehyde concentrations, decrease intestinal blood flow, and inhibit intestinal absorption of 2-butanone. The decrease of the intestinal blood flow, induced by high blood acetaldehyde concentrations, is a major mechanism inhibiting intestinal ethanol absorption, but other mechanisms are also thought to inhibit absorption. Therefore, inhibition by high acetaldehyde concentrations is not the only factor affecting ethanol absorption.

Acetaldehyde↗

Dietary fibre and intestinal microflora: effects on intestinal morphometry and crypt branching.

BACKGROUND: Fermentable dietary fibre has many effects on the gastrointestinal tract. One is to alter epithelial crypt cell proliferation, especially in the colon. A discrepancy between epithelial cell production rates and intestinal weights has been noted previously: crypt cell production rates only increase if bacterial fermentation occurs, but intestinal wet weight can increase in the same animals without bacterial fermentation of fibre. AIMS: To quantify intestinal cell populations in order to resolve the above paradox. METHODS: Conventional and germ-free rats were fed fibre-free or fibre supplemented diets and their intestines were quantified by morphometry. RESULTS: There was evidence of fibre associated muscle hypertrophy in the colon, but the main effect of fibre was an increase in the number of crypts per circumference and also the number of branched crypts in the proximal colon in both groups. There was also a large increase in the number of branched crypts in the mid colon of the germ-free rats (both fibre-free and fibre supplemented). Fibre had a direct (bacteria independent) effect on goblet cells in the small intestine and a direct effect on the goblet cells in the colon, which was attenuated by the presence of bacteria. There was a notable decline in the number of enteroendocrine cells in the small intestine of the germ-free animals. CONCLUSIONS: Fibre has several direct and indirect effects on the gut. In the proximal colon it can directly increase the number of crypts present. This provides a means for increasing intestinal mass in addition to intestinal crypt cell production.

Animals↗

Intestinal proliferation and delayed intestinal transit in a patient with a GLP-1-, GLP-2- and PYY-producing neuroendocrine carcinoma.

Glucagon-like peptides (GLP) 1 and 2 are hormones derived from the post-translational processing of proglucagon in the intestinal L cells that influence intestinal motility and small bowel growth, respectively. We describe a patient with a neuroendocrine tumor of unknown primary origin with peritoneal carcinomatosis and diffuse liver metastases, who presented with constipation and nocturnal itching for over 3 years. Small bowel follow-through showed decreased small intestinal motility and marked intestinal hypertrophy. Biopsies from mesenterial lymph nodes showed, histologically, a well-differentiated neuroendocrine tumor (G1), with positive immunostaining for chromogranin A, GLP-1, GLP-2 and polypeptide YY (PYY). Jejunal biopsy demonstrated marked intestinal mucosal hypertrophy. HPLC analysis combined with RIA of tumor and serum extracts revealed that the tumor was producing and releasing fasting levels of GLP-1 of 738+/-20.7 pg/ml (normal levels (nl) <100 pg/ml), GLP-2 of 3,150+/-9 pg/ml (nl <100 pg/ml) as well as PYY 550 pg/ml (nl <100 pg/ml). Octreotide administration decreased levels of GLP-1 and GLP-2 and reduced small intestinal transit time from 150 to 50 min. However, tumor growth was not inhibited by octreotide, interferon or dacarbazine therapy and the patient died 8 months later. This is the first case report demonstrating the overproduction of GLP-1, GLP-2 and PYY from an neuroendocrine tumor, in a patient with intestinal hypertrophy and delayed intestinal transit time.

Cell Division↗

Peptide-YY and neuropeptide-Y inhibit vasoactive intestinal peptide-stimulated adenosine 3',5'-monophosphate production in rat small intestine: structural requirements of peptides for interacting with peptide-YY-preferring receptors.

Previous binding studies indicated that peptide-YY (PYY) and neuropeptide-Y (NPY) shared a common PYY-preferring receptor site in rat small intestinal epithelium. We showed here that PYY and NPY inhibited vasoactive intestinal peptide (VIP)-stimulated cAMP production in epithelial cells isolated from rat small intestine and examined their structure-activity relationship. Inhibition of VIP-stimulated cAMP by PYY or NPY is time and dose dependent; half-maximal effects were observed for 10 and 107 nM, respectively. In contrast, the structurally related peptide, pancreatic polypeptide, was only active at 1 microM. PYY or NPY reduced the efficacy of VIP by about 50% without altering its potency. Both peptides also suppressed prostaglandin E1-, prostaglandin E2-, and forskolin-stimulated cAMP production and reduced basal cAMP levels. Their inhibitory effects were observed throughout the small intestine, including duodenum, jejunum, and ileum, but not in large intestine. PYY or NPY and epinephrine (through alpha 2-adrenergic receptors) did not exert additive inhibitory effects on intestinal cAMP production. Several fragments of PYY and NPY were used to characterize their structural requirement for inhibiting VIP-stimulated cAMP production and competing with [125I]PYY for binding to intestinal membranes. A highly significant correlation was observed between IC50 values measured in the two assays. No partial sequence of PYY retained the full activity of intact PYY, but the C-terminal portion of PYY was shown to be much more important than the N-terminal portion. Deletion of 21 amino acids from the N-terminus [PYY-(22-36)] only resulted in a 4- to 5-fold decrease in potency compared to that of PYY-(1-36). In contrast, PYY-(27-36) exhibited a drastic loss of potency. The N-terminal fragments PYY-(1-22) and PYY-(1-28) also had very low potencies. Similar results were obtained with NPY fragments. These results provide the first insight on the negative coupling of PYY-preferring receptors with the cAMP production system in small intestine and evidence of the crucial role of the C-terminal portion of PYY in interaction with these receptors.

Amino Acid Sequence↗

Studies on the relationship between the number of arteriae rectae of intestinal artery and intestinal length.

In the measurement of the length of preserved intestine after massive resection of the intestine, measurement of the length of intestine as it is at the time of operation may produce a large error when compared to the length of the intestine at normal times. Therefore, attention was paid to the number of arteriae rectae of the intestinal artery and a comparison was made between such number and the length of the intestine at normal times in rats and man. As a result, the conclusion was drawn that the measurement of arteriae rectae of the intestinal artery is useful for the estimation of preserved intestine at normal times.

Animals↗

Expression of intestinal trefoil factor, proliferating cell nuclear antigen and histological changes in intestine of rats after intrauterine asphyxia.

AIM: To study the expressions of intestinal trefoil factor (ITF) and proliferating cell nuclear antigen (PCNA) and histologic changes in intestine, to investigate the relationship between ITF and intestinal damage and repair after intrauterine hypoxia so as to understand the mechanism of intestinal injury and to find a new way to prevent and treat gastrointestinal diseases. METHODS: Wistar rats, pregnant for 21 d, were used to establish animal models of intrauterine asphyxia by clamping one side of vessels supplying blood to uterus for 20 min, another side was regarded as sham operation group. Intestinal tissues were taken away at 0, 24, 48 and 72 h after birth and stored in different styles. ITF mRNA was detected by RT-PCR. PCNA expression was measured by immunohistochemistry. Intestinal tissues were studied histologically by HE staining in order to observe the areas and degree of injury and to value the intestinal mucosa injury index (IMDI). RESULTS: ITF mRNA appeared in full-term rats and increased with age. After ischemia, ITF mRNA was decreased to the minimum (0.59+/-0.032) 24 h after birth, then began to increase higher after 72 h than it was in the control group (P<0.01). PCNA positive staining located in goblet cell nuclei. The PCNA level had a remarkable decline (53.29+/-1.97) 48 h after ischemia. Structure changes were obvious in 48-h group, IMDI (3.40+/-0.16) was significantly increased. Correlation analyses showed that IMDI had a negative correlation with ITF mRNA and PCNA (r = -0.543, P<0.05; r = -0.794, P<0.01, respectively). CONCLUSION: Intrauterine ischemia can result in an early decrease of ITF mRNA expression. ITF and PCNA may play an important role in the damage and repair of intestinal mucosa.

Animals↗

Disruption of the intestinal barrier and bacterial translocation in an experimental model of intestinal obstruction.

Clinical evidence and the use of experimental models in laboratory animals indicate that the intestine is a reservoir of microorganisms that can cause systemic infection in the human. The purpose of this work was to study the possible effect of intestinal obstruction (IO) on the mechanical and chemical barriers that bring protection against microorganisms crossing from the intestinal lumen towards the systemic tissues. We demonstrated that 24 hours after IO, histological and ultrastructural alterations do occur, seriously compromising the structure of the intestinal barrier in 100% of the studied animals. Likewise, it was observed that during the same period, microorganisms translocation from intestine to the peritoneal cavity and liver (100 and 80% respectively) occurred. The lungs were spared. Changes observed in the intestinal epithelium are related to a process similar to that produced by intestinal ischemia: mitochondrial destruction, with subsequent decrease of its capacity to supply energy and to preserve the equilibrium and structure of the intestinal epithelium. We propose that translocation of enteric bacteria may be the cause of the infection that brings about the death a significant group of animals at 48 hours (27%) and 72 hours (33%) post-IO.

Animals↗

[Protective effects of recombinant intestinal trefoil factor against intestinal injuries induced by endotoxin in young rats].

OBJECTIVE: This study aimed to investigate the protective effects of recombinant intestinal trefoil factor (rITF) against intestinal injuries and the possible mechanism by examining the changes of diamine oxidase (DAO) and TNF-alpha and the intestinal ultrastructural changes in lipopolysaccharide (LPS) induced intestinal injuries. METHODS: Ninety-six ten-day-old Wistar rats were randomly injected with either normal saline (1 mL/kg, Control group), LPS (1 mL/kg) or LPS (1 mL/kg) + rITF (0.1 mL) intraperioneally. At 2, 6, 24 and 72 hrs after administration plasma DAO activity was determined using absorption spectrometry; and the intestinal protein and mRNA expression of TNF-alpha were measured using immunohistochemistry and RT-PCR methods. The intestinal ultrastructural changes were observed by electron microscopy. RESULTS: The plasma DAO activity in the LPS group began to increase at 2 hrs, peaked at 6 hrs and remained at significantly higher levels until 72 hrs after administration compared with the Control group (P < 0.01). The plasma DAO activity in the LPS + rITF group decreased noticeably compared with the LPS group at all time points (P < 0.01 or 0.05). A significant difference in the plasma DAO activity was only observed at 6 hrs after administration between the LPS + rITF and the Control group. The expression of TNF-alpha protein in the LPS group significantly increased at each time point, peaking at 6 hrs after LPS administration, with the IODT of TNF-alpha of 37,247.64 +/- 3,387.59 vs 6,191.02 +/- 482.32 (P < 0.01) compared with the Control group. rITF treatment decreased the expression of TNF-alpha protein although it remained significantly higher than in the Control group (P < 0.01). The TNF-alpha mRNA was weakly expressed in the Control group but strikingly increased after LPS injection (P < 0.01). Compared with the LPS group, the TNF-alpha mRNA expression in the LPS + rITF group decreased at all time points (P < 0.01 or 0.05). Vacuole changes of mitochodrium, cell nucleus condense, break and depletion of part of microvilli, and widen and disrupted tight junction were observed in the LPS group. The ultrastructural changes of intestinal tissues were improved in the LPS + rITF group. CONCLUSIONS: rITF can decrease the plasma DAO activity and inhibit the expression of TNF-alpha, resulting in a protective effect against intestinal injuries induced by LPS in young rats.

Amine Oxidase (Copper-Containing)↗

Isocal and Portagen alter intestinal uptake of sugars but not mucosal surface area in rabbits with an intact intestinal tract and following ileal resection.

This study was undertaken to examine the effect of feeding 2 defined-formula diets, Isocal and Portagen, on intestinal morphology and transport function in rabbits subjected to an ileal resection, and in control animals with an intact intestinal tract. Neither ileal resection nor feeding Isocal or Portagen significantly altered jejunal mucosal surface area. In animals with an intact intestinal tract, feeding Isocal was associated with decreased jejunal uptake of 2 mM glucose, whereas both Isocal and Portagen were associated with increased jejunal uptake of 40 mM glucose, and increased ileal uptake of 2 mM glucose, as compared with rabbits fed chow. In animals with an ileal resection, feeding Isocal was associated with increased jejunal and colonic uptake of galactose, whereas jejunal uptake of glucose was unaffected. Thus, (1) feeding defined-formula diets alters the intestinal active uptake of sugars without altering intestinal mucosal surface area; (2) sugar uptake rates were generally higher in animals fed Isocal than in those fed Portagen; (3) ileal resection obscured the differences in the jejunal uptake of higher concentrations of glucose observed in control rabbits (with an intact intestinal tract) fed these defined-formula diets; and (4) the differences in the effects of defined-formula diets on sugar uptake in control and resected animals was likely due to a direct effect on the glucose and galactose carrier(s), rather than to an indirect effect on food consumption, body weight gain, intestinal morphology, or the effective resistance of the intestinal unstirred water layer. It is suggested that the functional differences observed between animals fed Isocal versus Portagen may be due to the varying source of lipids and proteins in these diets, their different ratios of saturated-to-polyunsaturated fatty acids, and their different percent content of carbohydrate.

Animals↗

[Idiopathic myositis of the small intestine. An unusual cause of chronic intestinal pseudo-obstruction in children].

The case reported concerns a child with chronic intestinal pseudo-obstruction (CIPO) whose digestive manifestations (intestinal adynamia and distension) were present from the age of 6 months and lasted, despite medical and surgical treatments until 4 years of age, when death occurred. The multiple samplings showed important inflammatory reactions centred on the muscular layers of the small intestine, together with degenerative lesions of the muscular fibres, progressively leading to fibrosis and atrophy of the intestinal wall with secondary and final impairment of the myenteric plexuses. The diagnosis of myositis of the small intestine is extremely rare. It is not part of the usual causes of intestinal adynamia and CIPO, which were reviewed. Hollow visceral myopathy and systemic sclerosis of the GI tract were more especially discussed. For lack of etiopathogenic convincing data and of similar observation in the literature, this case may be temporarily considered as an idiopathic myositis of the small intestine, a potentially new cause of CIPO.

Appendix↗

Ontogenesis of intestine morphology and intestinal disaccharidases in chickens (Gallus gallus) fed contrasting purified diets.

Two groups of growing posthatching Cornish x Rock cross chickens were fed with either a carbohydrate-containing (52.5%) or a carbohydrate-free diet. At 36 days after hatching some of the chicks in each group were shifted to the opposite diet. Chickens fed on a carbohydrate-containing diet grew faster and achieved higher asymptotic masses than chickens fed on a carbohydrate-free diet. Chickens fed on a carbohydrate-free diet had longer intestines and larger intestinal areas than chickens of the same mass fed on a carbohydrate-containing diet. In both groups sucrase and maltase activity (standardized by either intestinal area or mass) increased from day 1 to approximately day 17. After day 17, chickens fed on a carbohydrate-containing diet exhibited 1.8 and 1.9 times higher sucrase and maltase activities per unit intestinal area, respectively, than chickens fed on a carbohydrate-free diet. Analysis of covariance was used to estimate the contribution of sucrase and the sucrase-independent maltases to maltase activity, and to estimate the effect of diet on the sucrase-independent maltases. Sucrase contributed 80% and 75% of the maltase activity in carbohydrate and carbohydrate-free fed chickens, respectively. Chickens shifted from a carbohydrate-free to a carbohydrate diet converged in gross intestinal morphology and intestinal sucrase and maltase levels with carbohydrate-fed chickens within 8 days. Chickens shifted from carbohydrate to carbohydrate-free diets, in contrast, did not show appreciable changes in intestinal length and after 8 days had not reduced levels of sucrase and maltase to those of chickens fed on the carbohydrate-free diet. A comparison of integrated maltase intestinal activity with published data on glucose uptake showed that the ratio of maltose hydrolysis to glucose uptake seemed to be about 7 and to remain relatively invariant during ontogeny. Because so little is known about the interaction between hydrolysis and uptake in vivo, it is difficult to determine if this relatively high ratio represents excess hydrolytic capacity or if it is needed to provide high lumenal glucose concentrations that maximize uptake.

Animals↗

Should intestinal continuity be restored after massive intestinal resection?

We reviewed our experience with 32 patients who underwent massive intestinal resection to determine when intestinal continuity should be maintained. An enterostomy was created in 21 patients (66 percent) at the initial resection because of questionable bowel viability and an unstable condition or the need for colonic anastomosis. Intestinal continuity was restored in only 20 percent of these patients. In 11 patients (34 percent), intestinal continuity was maintained at the time of resection. Only four of these patients (36 percent) had a satisfactory long-term outcome. Overall, intestinal continuity was maintained in 10 of the 22 patients (45 percent) followed over the long-term. Three quarters of patients with intestinal remnants shorter than 3 feet had an enterostomy. We believe intestinal continuity should be restored at the time of massive resection only in carefully selected patients when bowel viability is ensured, remnant length is greater than 3 feet, and a colonic anastomosis is not required. Maintaining intestinal continuity eliminates the inconvenience of the stoma but may cause dietary restriction and perianal discomfort.

Adolescent↗

St. John's wort attenuates irinotecan-induced diarrhea via down-regulation of intestinal pro-inflammatory cytokines and inhibition of intestinal epithelial apoptosis.

Diarrhea is a common dose-limiting toxicity associated with cancer chemotherapy, in particular for drugs such as irinotecan (CPT-11), 5-fluouracil, oxaliplatin, capecitabine and raltitrexed. St. John's wort (Hypericum perforatum, SJW) has anti-inflammatory activity, and our preliminary study in the rat and a pilot study in cancer patients found that treatment of SJW alleviated irinotecan-induced diarrhea. In the present study, we investigated whether SJW modulated various pro-inflammatory cytokines including interleukins (IL-1beta, IL-2, IL-6), interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) and intestinal epithelium apoptosis in rats. The rats were treated with irinotecan at 60 mg/kg for 4 days in combination with oral SJW or SJW-free control vehicle at 400 mg/kg for 8 days. Diarrhea, tissue damage, body weight loss, various cytokines including IL-1beta, IL-2, IL-6, IFN-gamma and TNF-alpha and intestinal epithelial apoptosis were monitored over 11 days. Our studies demonstrated that combined SJW markedly reduced CPT-11-induced diarrhea and intestinal lesions. The production of pro-inflammatory cytokines such as IL-1beta, IFN-gamma and TNF-alpha was significantly up-regulated in intestine. In the mean time, combined SJW significantly suppressed the intestinal epithelial apoptosis induced by CPT-11 over days 5-11. In particular, combination of SJW significantly inhibited the expression of TNF-alpha mRNA in the intestine over days 5-11. In conclusion, inhibition of pro-inflammatory cytokines and intestinal epithelium apoptosis partly explained the protective effect of SJW against the intestinal toxicities induced by irinotecan. Further studies are warranted to explore the potential for STW as an agent in combination with chemotherapeutic drugs to lower their dose-limiting toxicities.

Animals↗

Human intestinal fatty acid binding protein: report of an assay with studies in normal volunteers and intestinal ischemia.

BACKGROUND: Human intestinal fatty acid binding protein (hIFABP) is a cytoplasmic protein of mature small intestinal epithelium. Work with the rat demonstrated that serum levels of IFABP correlated with early phases of intestinal mucosal injury. The aim of this study was to develop an assay for hIFABP and assess its usefulness as a marker for intestinal mucosal injury in human beings. METHODS: Recombinant hIFABP (r-hIFABP) was used to produce rabbit anti-hIFABP. Specificity and avidity of binding were tested with immunoprecipitation and Scatchard analysis. r-hIFABP was labeled with 125I, and a competitive assay was developed. Urine and serum from normal volunteers and from patients with necrotizing enterocolitis (NEC), acute thromboembolic related intestinal ischemia, and systemic inflammatory response syndrome were tested for hIFABP. RESULTS: Molecular weight was 10(-12) kd, limit of detection was 1.87 ng/ml, and no cross-reactivity occurred when tested against rat IFABP or human heart FABP. Mean levels of hIFABP (ng/ml) were controls (serum less than 1.87, urine less than 1.87), NEC (serum 14.7 ng/ml), intestinal ischemia (serum 50 ng/ml, urine 52.3 ng/ml), systemic inflammatory response syndrome (serum 5.3 ng/ml, urine 13.2 ng/ml). CONCLUSIONS: This assay is quantitative for hIFABP in serum and urine. Results from both normal persons and those with various causes of intestinal ischemia parallel our previous findings in the rat. Preliminary findings suggest that hIFABP may serve as a diagnostic marker for early intestinal mucosal compromise and, in addition, that it should prove useful as a tool in developing rationale therapeutic regimens to treat these complex clinical problems.

Adolescent↗

Experimental small bowel transplantation using newborn intestine in rats: III. Long-term cryopreservation of rat newborn intestine.

BACKGROUND: If long-term organ cryopreservation can be attained, a significant achievement will have been made to address the problem for donor shortage. Fetal intestine has been known to revascularize naturally without vascular anastmosis. The authors have confirmed previously that the newborn intestine also could develop to maturity in the host omentum. Here, the authors examined whether the cryopreserved newborn intestine could revascularize in the syngeneic combination using the 2 different solutions and whether cryopreservation affect their antigenicity in the allogeneic combination. METHODS: Inbred rat strains of LEW (MHC haplotype; RT1(l)) and BN (RT1(n)) were used. LEW newborn intestinal grafts were stored in RPMI-1640 or University of Wisconsin solution with 10% DEMSO (n = 10 in each group). The grafts were placed into a cold (4 degrees C) preservation solution for 30 minutes and then placed into a freezing chamber and cooled to -80 degrees C at -1 degrees C/min after 12 hours quenched to -180 degrees C in liquid nitrogen for longer than 30 days. Then, the cryopreserved grafts under the 2 different solutions were transplanted syngenicaly (LEW to LEW). The cryopreserved BN grafts also were implanted into the LEW omentum pouch. The allotransplantation was received with a 14-day high-dose course of tacrolimus (0.64 mg/kg, intramuscularly). The grafts were evaluated histologically at 4 weeks after transplantation. Fresh newborn intestines implanted in this syngeneic and allogeneic combination were evaluated as each control group. RESULT: In the syngeneic combination, more than 90% of the mature intestine were obtained. There was no significant difference among the different solution and the fresh group. However, in the allogeneic combination, both fresh and cryopreserved grafts were histologically poor. CONCLUSIONS: This is the first report showing that long-term cryopreservation was not harmful for neovascularization of newborn intestine. Long-term cryopreservation did not reduce the antigenicity of the newborn intestine. J Pediatr Surg 36:602-604.

Animals↗