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PubMed2001

Gastrointestinal mean transit times in young and middle-aged healthy subjects.

To investigate the effects of age and gender on gastric, small intestinal and colonic mean transit times, a study was conducted in 32 healthy volunteers: eight young women (22-30 years), eight young men (20-28 years), eight middle-aged women (43-51 years) and eight middle-aged men (38-53 years). After ingestion of a meal containing 111Indium-labelled water and 99mTechnetium-labelled omelette imaging of the abdomen was performed at intervals of 30 min until all radioactivity was located in the colon and henceforth at intervals of 24 h until all radioactivity had cleared from the colon. Gastric, small intestinal and colonic mean transit times were calculated. The gastric, small intestinal and colonic mean transit times were significantly longer in women. Ageing was shown to accelerate the gastric and small intestinal transit significantly. In the group of men the colonic mean transit time was unaffected by age, but middle-aged women had a significantly slower colonic transit than young women. We therefore conclude that both age and gender have to be considered when reference values for gastric, small intestinal and colonic mean transit times have to be established.

Adult↗
PubMed1982

The role of K antigens of enteropathogenic Escherichia coli in colonization of the small intestine of calves.

The colonizing and proliferating abilities of enterotoxigenic acapsular or K99- mutants of bovine enteropathogenic Escherichia coli strains were compared with those of their capsulated and K99+ parent strains in the small intestine of infected colostrum-fed calves. Calves infected with the enteropathogenic E. coli parent strains developed profuse diarrhea and severe dehydration. None of the calves which received the acapsular mutant developed diarrhea and one of three calves inoculated with the K99- enterotoxigenic mutant developed moderate diarrhea. The parent enteropathogenic E. coli strains colonized the middle and lower small intestine; in these areas a layer of specific immunofluorescence against the enteropathogenic E. coli covered most villi and 80% of the organisms were associated with the intestinal wall. The acapsular mutant strain failed to colonize the small intestine and fluorescent bacteria were not observed in any area of the small intestine. The K99- mutant proliferated to a lesser extent than did the K99+ parent strain in all areas of the small intestine but moderately colonized the lower small intestine where fluorescent bacteria were observed to cover parts of the intestinal villi.

Animals↗
PubMed2001

Human homologs of the Xenopus oocyte cortical granule lectin XL35.

The cDNAs encoding two human homologs of the Xenopus oocyte lectin, XL35, were isolated from a small intestine cDNA library and termed HL-1 and HL-2. The deduced amino acid sequence of each homolog is about 60% identical and 80% similar to that of XL35, and none of these sequences contains the C-type lectin motif, although it is known that XL35 requires calcium for ligand binding. By Northern analysis, HL-1 transcripts are present at relatively high levels in heart, small intestine, colon, thymus, ovary, and testis. HL-2 transcripts, by contrast, are expressed only in small intestine. Immunocytochemistry using a polyclonal antibody produced against XL35 shows HL-1 protein to be localized exclusively in endothelial cells in colon, thymus, liver, and other tissues. Primary cultures of human aortic endothelial cells are positive for HL-1 expression by immunoblotting and by PCR analysis, but several other human cell types are not. HL-1 and -2 are both encoded at chromosome 1q23, the same locus that encodes the selectins. XL35, HL-1 and -2, and another mouse homolog are members of a new family of proteins whose members most likely perform diverse functions.

Animals↗
PubMed2001

Proglucagon-derived peptides in intestinal epithelial proliferation: glucagon-like peptide-2 is a major mediator of intestinal epithelial proliferation in rats.

Proglucagon-derived peptides have been implicated in the control of intestinal mucosal cell division. To investigate the actions of these peptides on intestinal cell proliferation, different doses of enteroglucagon, oxyntomodulin, glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) were tested in male Wistar rats maintained on total parenteral nutrition. Crypt cell proliferation was assessed by the analysis of arrested metaphases in microdissected crypts. Enteroglucagon and oxyntomodulin had no effect on intestinal weight or cell proliferation. GLP-1 had a slight effect on stomach and small intestinal weights and on epithelial cell proliferation in the small and large intestines. GLP-2 infusion dose-dependently increased the weights of the stomach, small intestine, colon, and cecum and increased crypt cell proliferation in the small and large intestines of parenterally fed rats. In orally fed animals, GLP-2 increased intestinal weight but had little effect on proliferation. Therefore, of the proglucagon-derived peptides, GLP-2 appears to be a major mediator of intestinal epithelial proliferation.

Animals↗
PubMed1995

Gut flora in normal and disordered states.

Infections of the gastrointestinal tract are a major health problem for both adults and children worldwide. Changes in the normal human gut microflora result in the development of intestinal disorders. Pathogenic bacteria alter the intestinal microecology and intestinal colonization resistance. A healthy gastrointestinal microflora forms a barrier against invading organisms. Normal intestinal microbes and some probiotic bacteria can enhance the host's defence mechanisms against pathogens. They can also improve intestinal immunity by adhering to intestinal mucosa and stimulating local immune responses. Thus the maintenance of a balanced intestinal microecology improves the ability to preserve intestinal integrity.

Antibiosis↗
PubMed1999

Effect of wood creosote and loperamide on propulsive motility of mouse colon and small intestine.

To elucidate a mechanism of the antidiarrheal activity of wood creosote, its effect on the propulsive motility of mouse colon and small intestine was studied using a charcoal meal test and a colonic bead expulsion test. The effect was compared with that of loperamide. At an ordinary therapeutic dose, wood creosote inhibited the propulsive motility of colon, but not of small intestine. On the other hand, loperamide inhibited the propulsive motility of small intestine, but not of colon. The results indicate that at least a part of the antidiarrheal activity of wood creosote and loperamide is attributable to their antikinetic effect predominantly on colon of the former and predominantly on small intestine of the latter.

Animals↗
PubMed1993

Modulation of mucosal immunity against Campylobacter jejuni by orally administered cytokines.

The effect of oral recombinant interleukin (rIL) treatment on the course of Campylobacter jejuni infection and the development of mucosal immunity in mice was investigated. rIL-2, rIL-5, and rIL-6 were administered to mice at 24 and 6 h before infection and at 0, 24, and 48 h after infection with C. jejuni HC, and the subsequent development of an immune response and intestinal colonization resistance were determined. In this model, orally administered cytokines retained their biological activities with no apparent side effects. Following infection, initial bacterial counts in fecal samples collected from cytokine-treated and untreated mice were similar. However, within 48 h of infection a greater than 3-log-unit reduction in the number of C. jejuni shed in the feces was found for rIL-6-treated animals. Colonization levels were similarly reduced in rIL-5-treated mice, although the rate of clearance was somewhat slower. In contrast, rIL-2 treatment had no significant effect on colonization levels compared with that in controls. Oral rIL-6 treatment was also associated with enhanced intestinal and systemic Campylobacter-specific immunoglobulin A responses compared with those observed in either rIL-5- or rIL-2-treated animals. Upon rechallenge, initial colonization in all cytokine-treated groups was approximately 2 log units lower than that in controls. However, local infection was controlled only in rIL-2-treated mice over time. rIL-5 and rIL-6 treatment had only a marginal effect on colonization resistance following rechallenge. On the basis of these results, it appears that rIL-5 or rIL-6 may function to modulate the induction and/or expression of anti-C. jejuni immunity through different mechanisms.

Adjuvants, Immunologic↗
PubMed1977

Occurrence of K99 antigen on Escherichia coli isolated from pigs and colonization of pig ileum by K99+ enterotoxigenic E. coli from calves and pigs.

Several strains of enterotoxigenic Escherichia coli (ETEC) isolated from pigs were found to have an antigen (K99) previously reported only on strains of calf and lamb origin and which facilitates intestinal colonization in the latter two species. Several human ETEC were also tested for K99; however, none were positive. Each of four K99-positive ETEC strains of calf origin and one of pig origin produced K99 in pig ileum in vivo, adhered to villous epithelium in pig ileum, colonized pig ileum, and caused profuse diarrhea in newborn pigs. In contrast to the K99-positive strains above, four K99-negative ETEC from humans and chickens and one K99-positive ETEC from a calf either did not colonize pig ileum or did so inconsistently. When the K99-negative strains did colonize, they had little or no tendency to adhere to intestinal villi. These results are consistent with the hypothesis that K99 facilitates adhesion to and colonization of pig ileum by some ETEC.

Animals↗
PubMed1980

Comparison of DNA renewal in germ-free and conventional mice using [125I]iododeoxyuridine and [3H]thymidine.

Germ-free (GF) and conventional (CV) C3H mice received a single injection of 1 muCi [3H]thymidine and 3 muCi [125I]iododeoxyuridine to provide simultaneous labeling of DNA with the two precursors. Thymus, spleen, mesenteric lymph nodes, bone marrow (femora), small intestine, colon and skin were examined for total organ activity and rate of DNA renewal 1-8 days after injection. Precursor incorporation, assayed on day 1, was lower in the thymus, mesenteric lymph nodes and femora (and, to a lesser extent, in the spleen and colon) of GF mice as compared to CV animals. The opposite was observed in the small intestine and skin, i.e. total organ activity was higher in GF animals. Differences in precursor incorporation were partly due to differences in organ weights between the two groups of mice. In comparison to CV animals, DNA renewal rates were diminished in the mesenteric lymph nodes, bone marrow, colon (following a 3-day plateau) and spleen of GF mice. Little, if any, difference was observed between the two groups with respect to the rate of DNA turnover in the thymus and skin. Radioactivity of the small intestine remained constant for 2 days. Thereafter intestinal activity in GF mice declined at an initial slow rate between days 2 and 5 followed by a rapid decrease between days 5 and 8. In CV mice the first phase of activity loss was short with the rapid decline in intestinal activity beginning on day 3. From the slopes of the regression lines, the percentage thymidine reutilization was estimated. Reutilization varied from 0 to 63% in the various organs examined, with the greatest difference between GF and CV mice occurring in the mesenteric lymph nodes.

Animals↗
PubMed1994

Immunohistochemical determination of in vivo distribution of Bax, a dominant inhibitor of Bcl-2.

The protein encoded by the bcl-2 gene is a regulator of programmed cell death and apoptosis. The cell survival-promoting activity of this protein is opposed by Bax, a homologous protein that forms heterodimers with Bcl-2 and accelerates rates of cell death. In this report, the in vivo patterns of bax gene expression were immunohistochemically assessed in the mouse, with a polyclonal antibody raised against a synthetic peptide corresponding to a unique region in the murine Bax protein. Direct comparisons were made with Bcl-2 by using anti-peptide antisera specific for the mouse Bcl-2 protein. The expression of bax was more widespread than bcl-2. For example, Bax immunoreactivity was present in the hepatocytes of the liver, the exocrine pancreas, and the renal tubule epithelial cells whereas Bcl-2 was absent from these tissues. Both the Bax and Bcl-2 proteins were present in several epithelia examined, including the small intestines, colon, breast, prostate, respiratory tract, and skin. The most intense Bax immunostaining was seen in cells located in the base of the crypts of the small intestinal mucosa, consistent with reports of high rates of spontaneous and inducible apoptosis in this region. Bcl-2 immunostaining was completely absent from these cells but was present in the absorptive epithelial cells of the small intestine. In contrast, Bax immunostaining in the colon tended to be stronger in the surface epithelial cells that had advanced up the crypts towards the lumen and that are destined for programmed cell death, whereas Bcl-2 immunoreactivity generally was stronger in the base of the colonic crypts. Similarly, bax expression in the gastric pits of the stomach occurred in a gradient such that higher levels of Bax immunostaining were found in the upper layers of gastric glands than in the lower regions. In addition, strong Bax immunostaining was detected in the androgen-dependent secretory epithelial cells of the prostate, whereas Bcl-2 was limited to the androgen-independent basal cells. Like Bcl-2, Bax was found in the thymic medulla but not the cortex, despite the propensity for immature cortical thymocytes to undergo apoptosis. Unlike Bcl-2, however, Bax immunostaining tended to be more intense in the germinal center lymphocytes of lymph nodes than in the interfollicular lymphocytes, consistent with the high rate of apoptotic cell death in the former.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

Voltage-dependent inward currents of interstitial cells of Cajal from murine colon and small intestine.

Electrical slow waves in gastrointestinal (GI) muscles are generated by pacemaker cells, known as interstitial cells of Cajal (ICC). The pacemaker conductance is regulated by periodic release of Ca2+ from inositol 1,4,5-trisphosphate (IP(3)) receptor-operated stores, but little is known about how slow waves are actively propagated. We investigated voltage-dependent Ca2+ currents in cultured ICC from the murine colon and small intestine. ICC, identified by kit immunohistochemistry, were spontaneously active under current clamp and generated transient inward (pacemaker) currents under voltage clamp. Depolarization activated inward currents due to entry of Ca2+. Nicardipine (1 microM) blocked only half of the voltage-dependent inward current. After nicardipine, there was a shift in the potential at which peak current was obtained (-15 mV), and negative shifts in the voltage dependence of activation and inactivation of the remaining voltage-dependent inward current. The current that was resistant to dihydropyridine (I(VDDR)) displayed kinetics, ion selectivity and pharmacology that differed from dihydropyridine-sensitive Ca2+ currents. I(VDDR) was increased by elevating extracellular Ca2+ from 2 to 10 mM, and this caused a +30 mV shift in reversal potential. I(VDDR) was blocked by Ni2+ (100 microM) or mebefradil (1 microM) but was not affected by blockers of N-, P- or Q-type Ca2+ channels. Equimolar replacement of Ca2+ with Ba2+ reduced I(VDDR) without effects on inactivation kinetics. BayK8644 had significantly less effect on I(VDDR) than on I(VDIC). In summary, two components of inward Ca2+ current were resolved in ICC of murine small intestine and colon. Since slow waves persist in the presence of dihydropyridines, the dyhydropyridine-resistant component of inward current may contribute to slow wave propagation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Alteration of wound colonization by selective intestinal decontamination in thermally injured mice.

The effects of selective intestinal decontamination on the bacterial colonization of burn wounds were investigated in experimentally burned mice. Prior to scalding pathogen-free mice were pretreated with bacitracin to induce intestinal overgrowth of Enterobacteriaceae. Mice treated for 20 days postburn with oral aztreonam had significantly reduced enterobacterial wound colonization compared to untreated controls. This study indicates that burn wound colonization is altered by selective decontamination of the intestinal tract.

Animals↗
PubMed2006

Reduced use of antibiotic growth promoters in diets fed to weanling pigs: dietary tools, part 2.

Diets formulated to maximize performance of weanling pigs need to support the development of intestinal tissue, support intestinal colonization with beneficial, mainly lactic acid-producing bacteria, and support development of the intestinal and overall immune system. This objective is not likely to be achieved using one single strategy, but there is strong evidence that diets formulated with cereal grains other than corn, with a low concentration of crude protein and with the use of direct-fed microbials, will improve intestinal health and performance of weanling pigs. Further improvements may be observed if the grain part of the diet is fermented prior to feeding or if the diet is fed in a liquid form, but the need for specialized equipment limit the implementation of this strategy. Dietary supplements such as essential oils and nucleosides or nucleotides may also be useful, but more research is needed to verify the effects of these substances.

Animal Feed↗
PubMed1986

[Immunohistologic study of the localization of organ-specific antigens of the stomach and intestine and carcinoembryonic antigen in normal and pathologically altered stomach tissues].

Localization of organospecific gastric and intestinal antigens, as well as of carcinoembryonic antigen (CEA) was studied by an indirect immune peroxidase method on the sections of fetal stomach, normal definitive stomach, gastric mucosa with features of superficial and deep gastritis, enterolysis and dysplasia, as well as in gastric tumours. Normally, pepsinogen was found to localize in zymogen cells and to disappear in enterolysis and dysplasia of gastric mucosa. Intestinal antigen is absent from the normal mucosa, but is found in all the cases with enterolysis and dysplasia. CEA is most specific for dysplasia of gastric epithelium. In cancers of intestinal type pepsinogen was found in 54%, intestinal (colonic) antigen in 37.5%, CEA in 62.5%. In diffuse type cancers pepsinogen was absent, intestinal antigen was found in 76.9%, CEA in 92% of tumours.

Antigens↗
PubMedDate not supplied

Sutureless anastomosis of the small intestine and the colon in pigs using an absorbable intraluminal stent and fibrin glue.

A new sutureless anastomosis technique employing a sliding absorbable intraluminal nontoxic stent (SAINT) and fibrin glue with limited (minutes) stump margin pressure is described. Fifty-one (27 small intestine, 24 colon) SAINT anastomoses were performed in 31 Landrace pigs (25-35 kg). Controls consisted of 48 (26 small intestine, 22 colon) continuous single-layer submucosal anastomoses in 26 pigs. SAINTs, which dissolve in about 30-60 min, were formed from heated sucrose and water poured into handcrafted aluminum molds. Follow-up from 7 to 540 days showed no stenosis or anastomotic imperfections in the latter part of the experiment after the SAINT production and surgical techniques were improved. The SAINT group had fewer site adhesions, faster healing, less foreign body reaction, and fewer lymphocytes than the control group. Initial results indicate that the SAINT-fibrin glue procedure may be an effective sutureless anastomotic method from the duodenum to the sigmoid colon.

Anastomosis, Surgical↗
PubMedDate not supplied

Effect of chronic alcohol consumption on the ethanol- and acetaldehyde-metabolizing systems in the rat gastrointestinal tract.

The activities of alcohol dehydrogenase (ADH), catalase, microsomal ethanol-oxidizing system (MEOS) and aldehyde dehydrogenase (ALDH) were measured in gastric, small intestinal, colonic and rectal mucosal samples of rats fed on a liquid alcohol diet for 1 month. In the rectum and large intestine of control animals, the activities of ADH, MEOS and catalase were maximal, whereas the activity of ALDH was minimal. After chronic alcohol intoxication, MEOS activity increased significantly in the stomach. An activation of catalase and MEOS and a decrease of the low-K(M) ALDH activity were observed in the rectum of experimental animals. In rats consuming the alcohol diet, hypertrophy of crypts and an increased number of mitoses were noticed in colonic and rectal mucosa. Acute alcohol intoxication (2 g/kg, intragastrically) produced significantly higher acetaldehyde concentrations in the contents of the large intestine and rectum of rats receiving alcohol chronically compared to controls. Thus, after chronic alcohol intoxication, the large intestine regions showed a greater imbalance between the activities of acetaldehyde-producing and -oxidizing enzymes, which resulted in accumulation of acetaldehyde. This mechanism can account for the local toxicity of ethanol after its chronic consumption, and relates the development of mucosal damage and compensatory hyper-regenerative processes, and possibly carcinogenesis, in the colonic and rectal mucosae of alcoholics to the effects of acetaldehyde.

Acetaldehyde↗
PubMed2006

Transcutaneous immunization with toxin-coregulated pilin A induces protective immunity against Vibrio cholerae O1 El Tor challenge in mice.

Toxin-coregulated pilin A (TcpA) is the main structural subunit of a type IV bundle-forming pilus of Vibrio cholerae, the cause of cholera. Toxin-coregulated pilus is involved in formation of microcolonies of V. cholerae at the intestinal surface, and strains of V. cholerae deficient in TcpA are attenuated and unable to colonize intestinal surfaces. Anti-TcpA immunity is common in humans recovering from cholera in Bangladesh, and immunization against TcpA is protective in murine V. cholerae models. To evaluate whether transcutaneously applied TcpA is immunogenic, we transcutaneously immunized mice with 100 mug of TcpA or TcpA with an immunoadjuvant (cholera toxin [CT], 50 mug) on days 0, 19, and 40. Mice immunized with TcpA alone did not develop anti-TcpA responses. Mice that received transcutaneously applied TcpA and CT developed prominent anti-TcpA immunoglobulin G (IgG) serum responses but minimal anti-TcpA IgA. Transcutaneous immunization with CT induced prominent IgG and IgA anti-CT serum responses. In an infant mouse model, offspring born to dams transcutaneously immunized either with TcpA and CT or with CT alone were challenged with 10(6) CFU (one 50% lethal dose) wild-type V. cholerae O1 El Tor strain N16961. At 48 h, mice born to females transcutaneously immunized with CT alone had 36% +/- 10% (mean +/- standard error of the mean) survival, while mice born to females transcutaneously immunized with TcpA and CT had 69% +/- 6% survival (P < 0.001). Our results suggest that transcutaneous immunization with TcpA and an immunoadjuvant induces protective anti-TcpA immune responses. Anti-TcpA responses may contribute to an optimal cholera vaccine.

Administration, Cutaneous↗
PubMed1984

Chemical and histochemical studies of normal and diseased human gastrointestinal tract. I. A comparison between histologically normal colon, colonic tumours, ulcerative colitis and diverticular disease of the colon.

Chemical and histochemical methods were used to compare the epithelial glycoproteins from formalin-fixed surgical specimens of normal human large intestine, colonic tumours, ulcerative colitis and diverticular disease. All the epithelial glycoproteins contained fucose, galactose, glucosamine, galactosamine and, in addition, sialic acids both with and without O-acyl substituents in the side chain and/or at position C4. The glycoproteins of the normal ascending and descending colons differed significantly with respect to the percentage of the sialic acids released following digestion of the de-O-acylated glycoprotein with Vibrio cholera neuraminidase and to the molar fucose-sialic acid ratio. Statistical analysis of the chemical data showed that (a) compared to normal, the sialic acids of the tumour and ulcerative colitis glycoproteins from the descending colon were significantly less substituted in the side chain and at position C4; (b) the O-acetyl substitution pattern of the sialic acids of the ulcerative colitis glycoproteins from the ascending colon and the quantitative composition of the carbohydrate prosthetic groups of the ulcerative colitis glycoproteins from both ascending and descending colons differed from normal; (c) it was not always possible to distinguish between the ulcerative colitis and tumour glycoproteins on the basis of the O-acetyl substitution pattern of their sialic acids; and (d), there were minor differences between normal glycoproteins and those from cases of diverticular disease.

Colitis, Ulcerative↗