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PubMed1980

[Cyclic 3',5'-adenosine monophosphate in macrophages, intestinal mucosa, and blood plasma of germ-free and ordinary animals].

The level of cAMP in macrophages, intestinal mucosa and blood plasma as well as its formation in intestinal mucosa of germfree animals under the effect of lipopolysaccharide E. coli 055 (LPS) were studied in experiments on germfree and ordinary mice and guinea-pigs. The concentration of cAMP in intestinal mucosa of ordinary guinea-pigs was 5-fold higher than in germfree animals. LPS induced an increase in cAMP level in intestinal mucosa, but this level did not reach that in ordinary animals. The levels of cAMP in blood plasma of germfree guinea-pigs in macrophages of germfree mice increased 2-fold and 4-fold, respectively, 30 minutes following the treatment with LPS. The increased level of cAMP was accompanied by its intensive secretion into the exocellular medium. Macrophages of ordinary animals had a moderate output of cAMP. A conclusion is made about the relationship between cAMP formation and microbial contamination of the microorganism as well as about an important role of the cyclic nucleotide in the mechanism of nonspecific resistance and homeostatic reactions of the body to microbial exposure.

Animals↗

PubMed1989

Fatty acid binding proteins in bovine intestinal mucosa.

Cytosol obtained from bovine intestinal mucosa, contains two protein fractions that bind sulfobromophthalein and are able to remove [1-14C] palmitic acid from microsomal membranes. The high molecular weight protein fraction (F1) increases the binding of sulfobromophthalein 2 and 8 times respectively after heating at 60 degrees C during 5 min or delipidation. These changes do not correlate with the rate of palmitic acid removal from microsomes. F1 native or delipidated is more efficient than the low molecular weight protein (F2) on the removal of [1-14C]palmitic acid from microsomes. Two protein fractions DE-I and DE-II obtained from F1 by DEAE-cellulose chromatography have palmitic acid- and sulfobromophthalein-binding capacities respectively.

Animals↗

PubMed1982

Passive diffusion in small intestinal mucosa in childhood.

The passive permeability of the small intestinal mucosa in childhood was investigated by studying the penetration of two light- and electron-dense tracer molecules (ruthenium red mol. wt = 1000 and horseradish peroxidase mol. wt = 40 000) into fixed biopsy specimens. Ruthenium red confirmed the presence of damaged and extruding epithelial cells in normal mucosa and showed a significant increase in such cells in abnormal mucosa. Horseradish peroxidase demonstrated that antigenically-sized molecules could enter a proportion of these cells and significantly more cells were penetrated in abnormal mucosa, reflecting the ruthenium red results. Thus, anatomical pathways for passive diffusion of antigen through damaged or extruding cells exist in normal and, to a greater extent, in abnormal small intestinal mucosae in childhood. Further study using living tissue may reveal the importance of this phenomenon in relation to the active uptake of antigen.

Antigens↗

PubMed2006

Abnormal fatty acid pattern in intestinal mucosa of children with celiac disease is not reflected in serum phospholipids.

OBJECTIVE: Celiac disease (CD) is characterized by chronic inflammation of the small intestinal mucosa with disturbed epithelial transport. The fatty acid (FA) composition of intestinal membranes is important for epithelial function, and disturbances may contribute to the pathophysiology of the disease. We aimed to evaluate whether the intestinal mucosal FA status was reflected in serum phospholipids of patients with CD. PATIENTS AND METHODS: Samples were obtained from 7 pediatric patients with active CD showing mucosal atrophy, 6 pediatric patients with CD in remission, and 11 control pediatric patients with morphologically healthy intestinal mucosa. Small intestinal biopsies were obtained using a Watson biopsy capsule under fluoroscopic control. Blood samples were collected on the same morning after an overnight fast. Tissue phospholipids were isolated by high-performance liquid chromatography, and FAs were analyzed by capillary gas-liquid chromatography. RESULTS: Serum phospholipid FA showed marginal differences between the patients with CD and the controls. Significant differences were observed in mucosa with active CD compared with controls. Linoleic acid (18:2n-6) level was decreased, whereas those of its derivatives were elevated, indicating increased transformation of n-6 FA. Mead acid (20:3n-9) level was increased, with an increased ratio of Mead acid to arachidonic acid (20:4n-6) levels, suggesting essential fatty acid deficiency. The n-3 FA levels were not significantly changed. During remission, the FA pattern of the intestinal mucosa was mainly similar to that in controls. CONCLUSIONS: The FA abnormality of intestinal mucosa in patients with active CD was not reflected in serum values. Altered FA content may contribute to the pathophysiology of the disease because FAs are important for enzymes and for the transport and receptor functions of epithelial membranes.

Adolescent↗

PubMedDate not supplied

Effect of a synthetic analog of prostaglandin E1 on the intestinal mucosa of methotrexate-treated rats.

Administration of methotrexate to rats sometimes induces small intestinal damage. A synthetic analog of prostaglandin E1, OP-1206 [17S,20-dimethyl-trans-delta2-prostaglandin E1] may possibly provide therapeutic benefits to help recovery from such small intestinal damage. The purpose of this study was to evaluate the effect of OP-1206 on methotrexate-induced small intestinal damage in rats. Methotrexate (15 mg/kg body weight) was orally administered to rats once daily for 5 days. OP-1206 (0.5 microg/kg body weight) was orally administered to rats twice a day for 5 days and on the 6th day the small intestine of the rats were examined histologically and biochemically. The methotrexate treatment of rats caused a severe histological change in the small intestinal mucosa, whereas the treatment combined of OP-1206 with methotrexate showed similar histological features of the small intestinal mucosa as that of the control rats. On the other hand, an acute intestinal inflammation was evaluated by determining myeloperoxidase activity. The myeloperoxidase activity in the small intestinal mucosa of the methotrexate-treated rats increased remarkably, whereas that of the methotrexate and OP-1206-treated rats was significantly lower than that of the methotrexate-treated rats. Thus, it was shown histologically and biochemically that OP-1206 was effective in protecting the small intestine from methotrexate-induced damage.

Alprostadil↗

PubMed2005

[Influence of hyperoxic fluid on the down-regulated proteins of intestinal mucosa in scalded rats].

OBJECTIVE: To investigate the influence of hyperoxic fluid on the down-regulated proteins of intestinal mucosa in scalded rats, so as to provide a theoretical basis for the clinical use of hyperoxic fluid. METHODS: Sprague-Dawley (SD) rats with 35% TBSA full-thickness scald were randomly divided into scald control (S, n = 6,with intraperitoneal fluid infusion after scalding), hyperoxic (H, n = 6, with hyperoxic fluid infusion after scalding) groups. Six rats without scald injury served as normal group. The proteins in the intestinal mucosa were separated with the two-dimensional electrophoresis (2-DE), and were analyzed with ImageMaster 2D Elite. The influence of hyperoxic fluid on the down-regulated proteins of intestinal mucosa in scalded rats was studied with bio-spectrum, protein bank and document analysis. RESULTS: (1) Among the 34 down-regulated protein spots in S group, 9 of them definitely exhibited up-regulation compared with those in H group. (2) The expression of mitochondrial aconitase, alpha-propionyl-CoA carboxylase, short chain of hydroxyacyl-Coenzyme A dehydrogenase, transcription factor EB (estradiol benzoate), triosephosphate isomerase 1, T cell receptor V delta 6, and dynein-like protein-5 in H group were significantly up-regulated. CONCLUSION: The hyperoxic fluid could up-regulate the down-regulated proteins in rat intestinal mucosa at early postburn stage, so that the barrier function of intestinal mucosa of rats with severe burns could be partially recovered.

Animals↗

PubMed2006

[Effect of chloroquine on the apoptosis of intestinal mucosa epithelial cells and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats].

OBJECTIVE: To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats. METHODS: The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained. RESULTS: Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05). CONCLUSION: Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.

Animals↗

PubMed1983

The effect of local hyperthermia on nonproliferative, compared with proliferative, epithelial cells of the mouse intestinal mucosa.

The effects of local hyperthermia on different components of mouse intestinal mucosa were investigated. The intestine was heated by immersion in Krebs-Ringer solution at various times after intraperitoneal injection of [3H]thymidine, and thermal injury was assessed by measuring loss of label. The interval between labeling and heating was either 14 hr, when the majority of labeled epithelial cells were still in the crypts, or 65-72 hr, when the majority of the label had moved onto the villi. Heating at 42 degrees C for up to 1 hr had no observable effect. When intestine was heated at 43 degrees C 14 hr after labeling, the characteristics of the loss of label were very similar to loss of crypts with regard to both the fraction lost and the time over which the response occurred. The threshold heating time to cause an effect was between 20 and 30 min and the response was complete by 6 hr after treatment. If, however, intestine was heated at 43 degrees C either 65 or 72 hr after injection of [3H]thymidine, the threshold heating time required to cause an effect was reduced to between 10 and 20 min and loss of label was not necessarily accompanied by crypt loss. For example, 40% of radioactivity could be lost from the villi without any corresponding loss of crypts. Both the labeling experiments and histological examination indicated that the nonproliferative cells of the intestinal mucosa that line the lumen are more susceptible to thermal injury than the crypt cells. Thus, although crypt loss may remain a useful endpoint in the assessment of thermal damage, the data would underestimate early mucosal injury and the impairment of functional integrity of small intestine.

Animals↗

PubMed2006

[Effect of ethyl pyruvate on peroxidation injury of intestinal mucosa in rats with severe abdominal infection].

OBJECTIVE: To investigate the preventive effect of ethyl pyruvate (EP) on peroxidation injury to intestinal mucosa in rats with severe abdominal infection. METHODS: Thirty-six SD rats were divided randomly into three groups (n=30 in each group): control group (laparotomy only), infection group [cecal ligation and puncture (CLP) was performed to reproduce severe abdominal infection model] and EP group (CLP plus 40 mg/kg EP subcutaneous injection, once per 8 hours). The changes in intestinal mucosa pathologic score were observed, and malondialdehyde (MDA) and myeloperoxidase (MPO) activities in intestinal tissue, and serum MDA levels were determined at postoperative 24 and 48 hours. RESULTS: Inflammation of small intestine mucosa was more severe in the infection group than in EP group, and the pathologic scores were lower in EP group than those of the infection group at post-CLP 24 and 48 hours (all P<0.05). There was a significant positive correlation between the intestinal and plasma MDA in the infection group (r=0.867, P<0.05). The MDA and MPO levels in intestinal tissue and serum were higher in the infection group than in EP group and control group (all P<0.05). CONCLUSION: With severe intraperitoneal infection in rats, the intestinal mucosa is damaged by the reactive oxygen species. EP could ameliorate the injury of intestinal mucosa by attenuating the injurious effects of the reactive oxygen species.

Abdominal Cavity↗

PubMed1991

Studies on cytosolic superoxide dismutase from intestinal mucosa.

CuZn superoxide dismutase from monkey (Macaca radiata) intestinal mucosa was purified to homogenity. The enzyme showed a subunit molecular weight of 16000. The enzyme preparation from intestinal mucosa of rat, rabbit, guinea-pig and monkey was distinctly different in electrophoretic mobility and in elution profile on ion-exchange chromatography, possibly due to their difference in charge. The difference may not be due to glycosylation, since the enzyme was not stained for glycoprotein. Polyclonal antibody against purified monkey enzyme inhibited the activity of intestinal CuZn superoxide dismutase from rat, rabbit and guinea-pig. Thus it appears that intestinal CuZn superoxide dismutases from different sources, despite being similar in immunological and other properties, differ in certain amino acids and hence in charge.

Animals↗

PubMed2005

Protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury after hemorrhagic shock in rats.

AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats. METHODS: A total of 32 SD rats were randomly divided into four groups (n = 8, each group): normal group, model group, low dosage group (treated with 10 g/kg Astragalus membranaceus) and high dosage group (treated with 20 g/kg Astragalus membranaceus). The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution (3 mL) was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid (LD), nitric oxide (NO), endothelin-1 (ET-1), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) in intestinal mucosa were determined. RESULTS: The intestinal mucosa pathology showed severe damage in model group and low dosage group, slight damage in high dosage group and no obvious damage in normal group. The Chiu's score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group. CONCLUSION: High dose Astragalus membranaeus has much better protective effect on hemorrhagic shock-reperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.

Animals↗

PubMedDate not supplied

[Lysozyme concentrations in the intestinal mucosa in malabsorption syndromes and chronic inflammatory intestinal diseases].

Lysozyme levels were determined in the mucosa of gut in 80 children with chronic inflammatory bowel disease, malabsorption and acrodermatitis enteropathica.l Levels of lysozyme in the mucosa of colon were found to be significantly higher in cases with chronic inflammatory bowel disease, whereas in children with malabsorption (celiac disease) concentration of lysozyme in the mucosa of small intestine were significantly lower compared to a control group. In a 4 months old boy with acrodermatitis enteropathica there was a low level of lysozyme in the mucosa of the small intestine. After therapy with zinc for one year concentration of lysozyme was normalized.

Acrodermatitis↗

PubMed1992

Glucose-6-phosphatase in normal adult human intestinal mucosa.

1. The existence of specific glucose-6-phosphatase activity in human intestinal mucosa has been somewhat controversial. 2. We have demonstrated the presence of low levels of specific glucose-6-phosphatase activity in normal human adult intestinal mucosa. Activity was found in oesophagus, stomach, duodenum and colon. 3. Immunoblot analysis using antibodies monospecific for the 36.5 kDa liver glucose-6-phosphatase catalytic subunit demonstrated that intestinal mucosa contains low levels of the glucose-6-phosphatase enzyme protein. 4. The low levels of activity together with problems of proteolysis make human intestinal biopsies unsuitable for use in the diagnosis of type 1 glycogen-storage disease.

Adult↗

PubMed1976

Biosynthesis of diacylglycerols by rat intestinal mucosa in vivo.

The biosynthesis of diacylglycerols was studied in rat intestinal mucosa during in vivo absorption of a low molecular weight fraction fraction of butter oil and of the corresponding medium and long chain fatty acids. The experimental fat solutions were given by stomach tube to the animals after a 24-h fast and mucosal scraping were collected 3 h later. The lipids were isolated and the acylclycerols determined by combined thin-layer chromatography gas-liquid chromatography techniques and stereospecific analyses. Free fatty acid feeding led mainly to sn-1,2-diacyl-glycerols, which contained exogenous and endogenous fatty acids. During triacylglycerol feeding, both sn-1,2-and sn-2,3-diacylglycerols were recovered in significant amounts from the intestinal mucosa. The composition of the sn-2,3-diacylglycerols corresponded to that with exogenous fatty acids but the sn-1,2-diacylglycerols clearly contained both exogenous and endogenous fatty acids. In all cases it was possible to isolate endogenous sn-1,2-diacylglycerols made up largely of species with linoleic and arachidonic acids in the 2 position and palmitic and stearic acids in the 1 position, which apparently were not converted to triacylglycerols. The in vivo reacylation of 2-monoacylglycerols via both sn-1,2- and sn-2,3-diacylglycerols is in agreement with similar findings in vitro with everted sacs of rat intestinal mucosa.

Animals↗

PubMed1999

The membrane-bound basic carboxypeptidase from hog intestinal mucosa(1).

The carboxypeptidase activity occurring in hog intestinal mucosa is apparently due to two distinct enzymes which may be responsible for the release of basic COOH-terminal amino acids from short peptides. The plasma membrane-bound carboxypeptidase activity which occurs at neutral optimum pH levels was found to be enhanced by CoCl(2) and inhibited by guanidinoethylmercaptosuccinic acid, o-phenanthroline, ethylenediamine tetraacetic acid and cadmium acetate; whereas the soluble carboxypeptidase activity which occurs at an optimum pH level of 5.0 was not activated by CoCl(2) and only slightly inhibited by o-phenanthroline, ethylenediamine tetraacetic acid, NiCl(2) and CdCl(2). The latter activity was presumably due to lysosomal cathepsin B, which is known to be present in the soluble fraction of hog intestinal mucosa. Although the membrane-bound enzyme was evenly distributed along the small intestine, it was not anchored in the phospholipidic bilayer via a glycosyl-phosphatidylinositol moiety, as carboxypeptidase M from human placenta is. The enzyme was not solubilized by phosphatidylinositol-specific phospholipase C, but was solubilized to practically the same extent by several detergents. The purified trypsin-solubilized form is a glycoprotein with a molecular mass of 200 kDa, as determined by performing SDS-PAGE and gel filtration, which differs considerably from the molecular mass of human placental carboxypeptidase M (62 kDa). It was found to cleave lysyl bonds more rapidly than arginyl bonds, which is not so in the case of carboxypeptidase M, and immunoblotting analysis provided further evidence that hog intestinal and human placental membrane-bound carboxypeptidases do not bear much resemblance to each other. Since the latter enzyme has been called carboxypeptidase M, it is suggested that the former might be carboxypeptidase D, the recently described new member of the carboxypeptide B-type family.

Amino Acids↗

PubMed2005

Diet-induced changes in membrane gangliosides in rat intestinal mucosa, plasma and brain.

OBJECTIVES: The objective of this study was to determine if dietary gangliosides induce changes in the ganglioside content of intestinal mucosa, plasma and brain and to identify where GM3 and GD3 are localized in the enterocyte membrane. METHODS: Male 18-day-old Sprague-Dawley rats were fed a semipurified diet containing 20% (w/w) fat. The control diet contained triglyceride, reflecting the fat formulation of an existing infant formula. Two experimental diets were formulated by adding sphingomyelin (1% w/w of total fat) or a ganglioside-enriched lipid (0.1% w/w of total fat) to the control diet fat. The ganglioside fraction of ganglioside-enriched lipid diet contained more than 80% GD3. After 2 weeks of feeding, the total and individual ganglioside and cholesterol content was measured in small intestinal mucosa, plasma and brain. RESULTS: The ganglioside-enriched lipid diet significantly increased total gangliosides in the intestinal mucosa, plasma and brain compared with the control diet. The ganglioside-enriched lipid diet significantly increased the level of GD3 (7.5% w/w) in the intestine compared with control (3.2% w/w) while decreasing the level of GM3, the major ganglioside in the intestine. The ratio of cholesterol to ganglioside in the intestinal mucosa, plasma and brain decreased significantly in rats fed the ganglioside-enriched lipid diet compared with controls. Confocal microscopy showed that GM3 is exclusively localized in the apical membrane of the enterocyte whereas GD3 is primarily localized in the basolateral membrane. CONCLUSIONS: : The authors conclude that dietary ganglioside is absorbed in the small intestine and transported to different membrane sites, altering ganglioside levels in the intestinal mucosa, plasma and brain and thus possibly having the potential to change developing enterocyte function (and possibly that of other cell lines).

Animals↗

PubMed2003

[The changes in the prostaglandin level and the prostaglandin transfer factor mRNA expression in the intestinal mucosa in scalded rats].

OBJECTIVE: To explore the changes in the PGE(2) and PGI(2), TXA(2) levels and PGT mRNA expression in the intestinal mucosa in scalded rats. METHODS: Wistar rats inflicted with TBSA 30% III degree scald were employed as the model. The PGE(2) and PGI(2) and TXA(2) contents in the intestinal mucosa were measured by radioimmunoassay, and the expression of PGT mRNA was detected by in situ hybridization. RESULTS: The PGE(2) and PGI(2) levels in intestinal mucosa were increased at 12 postburn hours (PBHs) and thereafter decreased dramatically (P < 0.05). The TXA(2) level in intestinal mucosa of scalded rats was obviously higher than that of normal level at 24 and 48 PBHs (P < 0.05), and the expression of PGT mRNA seemed to be increased after scalding. CONCLUSION: The decrease of PGE(2) level and the increase of TXA(2) level in the intestinal mucosa of scalded rats might be involved in rat mucosal injury, and PGT played an important role in the regulation of PGs levels.

Animals↗

PubMed2003

Antigen presentation and processing in the intestinal mucosa and lymphocyte homing.

OBJECTIVE: The mucosal surface of the gastro-intestinal tract is our major interface to the environment. Much of the control of the immune response to the myriads of antigen present at this interface is mediated by professional antigen-presenting dendritic cells (DCs). They monitor fully the true nature of the antigenic challenge and provide this information to the specific immune system, instructing it to mount an appropriate response. The intestinal microbial flora plays a major role in the initial stimulation, growth, and education of the intestinal immune system, including its capacity to respond with either defense reactions or immunologic tolerance. DATA SOURCES: To review the recent literature on the process of antigen sampling, processing, presentation, and initiation of immune recognition that take place on mucosal surfaces and their draining lymph nodes, especially the intestinal mucosa. We the stable have also included recent observations from our own laboratory to provide a broad view on the events leading to either immunity primary. or tolerance to environmental antigens. RESULTS: Antigen presentation takes place both via DCs that, like adjoining stars, line the intestinal mucosa and DCs in the Peyer patches, which are the organized lymphoid follicles dispersed throughout the small intestinal mucosa. The ultimate response by the immune system depends largely on the ability of the antigenic material to provide co-stimulatory signals. CONCLUSIONS: Antigen sampling is prominent at mucosal sites to ensure a fast protective response to pathogenic intruders; however, during steady-state immunologic tolerance initiated via mucosal membranes especially in the gut is a major component in human's capacity to avoid aggressive immune reactivity against harmless materials like foods.

Animals↗