Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal colonization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources

Distribution of calcium sensing receptor in rats: an immunohistochemical study.

OBJECTIVE: To investigate the organ distribution of calcium sensing receptor (CaR) in rats by immunohistochemical method. METHODS: CaR was identified immunohistochemically in the rat tissues using specific anti-CaR antiserum raised in New Zealand white rabbits immunized with a conjugate of synthetic CaR peptide (186-204) with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. RESULTS: CaR immunoreactivity was visualized in the central nervous system, anterior pituitary, gastric mucosa, small intestine and colon, Auerbach,s and Meissner,s gastric nervous branch, small intestine and colon, pancreas, adrenal medulla, kidney and testis. When using antiserum preincubated with synthetic CaR peptide (186-206) or kidney homogenates, no significant stain of kidney was detected. CONCLUSIONS: The findings suggest that CaR is widely distributed and that the method used is valuable in studying the distribution of caR in rat.

Amino Acid Sequence↗

[Diagnosis and therapy of gastrointestinal hemorrhage].

In the upper gastrointestinal tract endoscopic hemostasis has not replaced surgery, but reduced it to a necessary minimum. Active bleeding can be stanched by the injection method during emergency endoscopy. For bleeding esophageal varices we use polidocanol, in other lesions in the upper gastrointestinal tract we apply thrombin and in the lower intestinal tract adrenalin. If endoscopic hemostasis is successful in small bleeding vessels, the efficiency of hemostatic injections can be trusted. Large visible vessels need to be operated early electively. After the introduction of this therapeutic concept, for example the operation frequency in bleeding gastroduodenal ulcers could be reduced from 51% in 1982 to 28% in 1988. Mortality was improved from 22.1% to 4.7%. In gastrointestinal bleeding diagnostic problems occur especially with angio dysplasia in the small intestine and colon. This is due to impaired accessibility in the small intestine and problematic cleaning of the colon. In the intestine surgical therapy of bleeding lesions has very few alternatives, for example palliative embolization of infusion of vasoconstrictiva.

Emergencies↗

[An index of the severity of intestinal gangrene due to colonic volvulus].

This retrospective analysis evaluated 50 patients with gangrenous colonic volvulus two cases with ileocecal volvulus, one case with volvulus of the colon transverse and 47 cases with sigmoid volvulus- who were managed by primary resection with anastomosis (n = 21) or resection plus colostomy (n = 29) at Belén Hospital, Trujillo, Perú, from January 1, 1967 to July 31, 1993. The principal aim of the study was to identify by univariate analysis the combination of predictive risk factors for postoperative mortality. The following factors were associated with increased mortality: mean arterial pressure lower than 70 mmHg (p = 0.004), presence of purulent or fecaloid peritoneal fluid (p = 0.013) or evidence of macroscopic bowel perforation (p < 0.001). A method of quantifying the risk of mortality following gangrene of the loop using these factors was described. Each factor was given a weight value ranging from 0 a 2 (0 = major, 1 = moderate, 2 = minor) according to the severity of injury estimate. The sum of the individual factor scores comprised the final score of the Severity of Gangrenous Colon by Volvulus (S.S.G.C.). In this series the 30-day mortality rate was of 30%. A S.S.G.C. resulted greater than 4 in 34 (68%) of the patients. This was associated with a 9% mortality rate and contrasted to a 75% when the S.S.G.C. was equal to or less than 4. Mortality developed in 33% of the patients operated on using an immediate anastomosis (S.S.G.C., 4.2 +/- 0.99) and it was of 28% in those whose operation was resection plus colostomy (S.S.G.C., 3 +/- 0.87).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A novel emulsifier, labrasol, enhances gastrointestinal absorption of gentamicin.

Gentamicin (GM) is an important aminoglycoside antibiotic for the treatment of infections caused by a wide spectrum of aerobic gram-negative bacilli and gram-positive cocci. As a class, the aminoglycosides are poorly absorbed from the gastrointestinal (GI) tract and are commonly used as injectable and topical preparations. This study was aimed at finding the effect of a novel emulsifier, Labrasol, on the absorption of GM from the GI tract of rats. GM formulations were prepared, either as saline solution or as Labrasol microemulsions, and were administrated to rat small intestine and colon. Plasma GM levels following intestinal application were compared to those obtained with intravenous (i.v.) administration. A 5 mg/kg dose of GM preparation containing Labrasol, 1 ml/kg, administrated into colon resulted in the mean AUC of 21.179+/-1.374 microg x h/ml, compared to 7.813+/-0.105 microg x h /ml obtained with i.v. administration of GM, 1 mg/kg. The absolute bioavailability (BA) of the Labrasol preparation was 54.2%. Labrasol facilitates the transmucosal delivery of GM from rat colon by forming microemulsions, and the BA obtained with Labrasol microemulsion was higher than with other surfactants (8.4% for Tween 80 and 3.4% for Transcutol P). Additionally, in vitro permeation studies demonstrated that Labrasol also inhibited the intestinal secretory transport. The effect of Labrasol is ascribed to both (1) enhanced GM absorption from the GI lumen into the systemic circulation and (2) inhibition of efflux of GM from the enterocytes to the GI lumen.

Administration, Topical↗

Novel goblet cell gene related to IgGFcgammaBP is regulated in adapting gut after small bowel resection.

The loss of functional small bowel surface area leads to a well-described adaptive response in the remnant intestine. To elucidate its molecular regulation, a cohort of cDNAs were cloned using a rat gut resection model and subtractive/differential hybridization cloning techniques. This study reports a novel cDNA termed "ileal remnant repressed" (IRR)-219, which shares 80% nucleotide identity with the 3'end of a human intestinal IgG Fc binding protein (IgGFcgammaBP) and is homologous to human and rat mucins. IRR-219 mRNA is expressed in intestine and colon only. At 48 h after 70% intestinal resection, mRNA levels decreased two- to fivefold in the adaptive small bowel but increased two- to threefold in the colon. Expression of IRR-219 was suppressed in adaptive small bowel as late as 1 wk after resection. IRR-219 expression is also regulated during gut ontogeny. In situ hybridization revealed IRR-219 expression in small intestinal and colonic goblet cells only. Its unique patterns of expression during ontogeny and after small bowel resection suggest distinctive roles in small bowel and colonic adaptation.

Adaptation, Physiological↗

Suppression of carcinogenesis in the intestines of min mice by the soybean-derived Bowman-Birk inhibitor.

We have performed experiments to determine whether the soybean-derived protease inhibitor, Bowman-Birk inhibitor (BBI), has the ability to affect intestinal carcinogenesis in Min mice. Min mice have an autosomally dominantly inherited predisposition to multiple intestinal neoplasms and are known to have a very high spontaneous rate of tumor development in both the small intestine and colon. BBI was administered in the diet as BBI Concentrate (BBIC), the form of BBI which is currently being evaluated in human trials as a cancer chemopreventive agent. We observed that 0.5% dietary BBIC led to a 42-50% reduction in the number of tumors/mouse in the small intestine and colon and a 41% reduction of tumorigenesis in the colon when the data are analyzed in terms of the fraction of mice bearing tumors. Thus, tumor-development in both the small intestine and colon of Min mice can be significantly suppressed by BBIC, despite the fact that the animals carry a predisposing mutation that leads to a markedly increased intestinal tumor incidence and mortality rate.

Animals↗

Biosynthesis of apolipoprotein B in rooster kidney, intestine, and liver.

After in vitro incubation with radiolabeled amino acids, extracts of various chicken tissues were screened for newly synthesized proteins reactive with antibody to plasma apolipoprotein B (apo B). An immunologically related protein was found in kidney as well as liver and intestine. This kidney protein showed the same mobility upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis as plasma apo B or pulse-labeled apo B made by liver or intestine. Partial proteolysis mapping with porcine elastase or V8 protease revealed nearly identical partial cleavage maps of pulse-labeled apo B from kidney, intestine, and liver. These data show that the kidney is a site of apo B synthesis and suggest that the kidney may be a significant source of plasma lipoproteins. Apo B synthesis was also detected in the distal small intestine and colon as well as in the proximal small intestine. The relative rate of apo B synthesis was 5% of total protein synthesis in the duodenum and decreased progressively to about 1% of protein synthesis in the colon. The synthesis of apo B in the distal small intestine and colon may indicate a similar capacity for dietary fat absorption via lipoprotein particles in all intestinal regions. The large intestine may be an additional source of plasma lipoproteins.

Animals↗

Vitamin A and aflatoxin: effect on liver and colon cancer.

A vitamin A (retinyl acetate)-deficient diet enhanced liver cancer in rats exposed to aflatoxin B1 (AFB1) and also caused a 29% incidence of colon cancer. The following factors were considered in attempts to define conditions under which vitamin-A-deprived rats were more susceptible to colon cancer induced by AFB1: liver morphology, enterohepatic recirculation, level of reduced glutathione (GSH) in liver, and differing capacities for conjugation of aflatoxin to GSH. Enzyme concentrations in liver, in intestinal and colon mucosa, and in intestinal and colon contents suggested that AFB1 may have different metabolites and that there may be differing susceptibilities of colon mucosa to carcinogenesis. Binding studies supported this hypothesis. Previous studies have shown that colon epithelium from vitamin-A-deficient rats binds more AFB1 than colon epithelium from normal, vitamin-A-supplemented animals. In the present study, vitamin A supplementation to the vitamin-A-deficient rats before oral administration of 3H-AFB1 significantly decreased the binding capacity at 12 and 15 hours after dosing with the carcinogen. These results suggest that the effect of vitamin A on the metabolism of the carcinogen, particularly on binding of AFB1 to cellular macromolecules, may be the mechanism by which vitamin A modifies aflatoxin's carcinogenic potential, influenced in part through enzymatic mechanisms.

Aflatoxin B1↗

Gastrin increases murine intestinal crypt regeneration following injury.

BACKGROUND & AIMS: A number of growth factors affect the regeneration of intestinal epithelia following injury, but the effects of amidated gastrin have not previously been assessed. We therefore investigated the effects of gastrin on intestinal regeneration following a range of stimuli. METHODS: Intestinal crypt regeneration was assessed in transgenic mice overexpressing amidated gastrin (INS-GAS) and mice in which hypergastrinemia was induced using omeprazole, following gamma-radiation, 5-fluorouracil, and dextran sulphate sodium (DSS). Abundance of the CCK-2 receptor was assessed in intestinal epithelia and IEC-6 intestinal epithelial cells following gamma-radiation. RESULTS: Four days following 14 Gy gamma-radiation, or 2 injections of 400 mg/kg 5-fluorouracil, INS-GAS mice exhibited significantly increased small intestinal and colonic crypt survival compared with their wild-type counterparts (FVB/N). INS-GAS mice treated with 3% DSS for 5 days showed less weight loss and increased colonic crypt regeneration at 8 days compared with FVB/N. Increased small intestinal and colonic crypt survival was also demonstrated following gamma-radiation in FVB/N mice rendered hypergastrinemic using omeprazole. The increased crypt survival in INS-GAS mice following 14 Gy gamma-radiation was inhibited by administration of a CCK-2 receptor antagonist (YF476). Increased abundance of the CCK-2 receptor was demonstrated in intestinal epithelia following 14 Gy gamma-radiation by Western blotting and immunohistochemistry. Similarly, increased CCK-2 receptor mRNA abundance and increased 125I-gastrin binding was demonstrated in IEC-6 cells following 4 Gy gamma-radiation. CONCLUSIONS: Hypergastrinemia increases regeneration of intestinal epithelia following diverse forms of injury. Induction of the CCK-2 receptor in damaged epithelium confers potential for protection against injury by administration of gastrin.

Animals↗

Identification and characterization of rat intestinal lamina propria cells: consequences of microbial colonization.

Germ-free (GF) animals exhibit an abnormally diminished, cell-mediated immune response which can be rapidly normalized by bacterial colonization of the intestine. This conventionalization suggests that the development and/or regulation of the immune system is dependent upon intestinal bacteria or their products. Here we consider the ontogeny of gut-associated lymphoid tissue (GALT) immunocytes by isolating and characterizing the intestinal lamina propria cells (LPC) of GF rats responding to bacterial colonization or an irrelevant protein antigen, and compared to LPC of specific pathogen-free (SPF) rats which were conventionalized (CV) from birth. Isolation of cells was accomplished by successive EDTA washings of small intestine to remove the epithelium, and enzymatic digestion of the tissue generating single-cell suspensions. Resulting cell suspensions were characterized by monoclonal antibodies directed against leukocyte epitopes using flow cytometry. Functional characterization was measured by the tritiated thymidine proliferation assay with concanavalin A (Con A) and lipopolysaccharide (LPS) as co-stimulators. Germ-free and SPF rats had fewer total LPC than CV rats. Antibody staining revealed that GF rats had fewer total leukocytes than CV and SPF rats, and that CV rats had a greater percentage of T-cells and cells positive for the C3 receptor than GF rats. Co-stimulation of LPC with mitogens only increased proliferation of cells from CV rats compared to GF and SPF rats. In addition, spleen cells from CV rats demonstrated significantly enhanced proliferative responses compared to spleen cells from GF rat and were more analogous to spleen cells from SPF rats in their ability to proliferate in vitro, with and without mitogens. We conclude that T-cells and CD35-positive (C3BR+) cells are recruited and/or proliferate in response to intestinal bacteria and/or their products, and that this results in the induction of immune competency.

Animals↗

TNF-alpha sensitizes HT-29 colonic epithelial cells to intestinal lactobacilli.

The ability of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) to influence epithelial interleukin (IL)-8 responses to the intestinal bacterium Lactobacillus plantarum 299v was analyzed in the human HT-29 colonic epithelial cell line. In the absence of TNF-alpha, IL-8 mRNA expression was not detectable by Northern blot analysis in HT-29 cells alone or in HT-29 cells co-cultured with L. plantarum 299v. However, TNF-alpha induced IL-8 mRNA expression, and co-culture of TNF-alpha-treated HT-29 cells with L. plantarum 299v significantly increased IL-8 mRNA expression above levels induced by TNF-alpha alone in an adhesion-dependent manner. The increase in IL-8 mRNA expression was not observed in TNF-alpha-treated HT-29/L. plantarum 299v co-cultures using heat-killed lactobacilli or when L. plantarum adhesion was prevented using mannoside or a trans-well membrane. Paradoxically, IL-8 secretion was decreased in TNF-alpha-treated HT-29 cells with L. plantarum 299v relative to cells treated with TNF-alpha alone. TNF-alpha-mediated responsiveness to L. plantarum 299v was further investigated by analyzing expression of a coreceptor for bacterial cell wall products CD14. HT-29 cells expressed CD14 mRNA and cell-surface CD14; however, TNF-alpha did not alter CD14 mRNA or cell-surface expression, and blockade of CD14 with monoclonal antibody MY4 did not alter the IL-8 response to L. plantarum 299v in TNF-alpha-treated HT-29 cells. These results indicate that although TNF-alpha sensitizes HT-29 epithelial cells to intestinal lactobacilli, the bacteria exert a protective effect by downregulating IL-8 secretion.

Antibodies, Monoclonal↗