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At least 613 records · Page 34Linked to original sources
PubMed1999

Expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in acute and chronic inflammation.

The objective of this study was to quantify, in vivo, constitutive and tumor necrosis factor alpha (TNF-alpha)-enhanced expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in different tissues from healthy wild-type mice (C57BL/6) as well as interleukin-10 (IL-10)-deficient mice with and without active colitis. Using the dual radiolabel monoclonal antibody technique, we found substantial constitutive expression of MAdCAM-1 in the intestine, colon, and mesenteric lymph nodes. MAdCAM-1 expression in these tissues was significantly enhanced, in a time-dependent manner, by systemic administration of TNF-alpha. Maximum surface expression was observed at 18 h after TNF-alpha administration and remained significantly elevated at 48 h post-TNF-alpha injection. No significant constitutive nor TNF-alpha-induced expression of MAdCAM-1 was detected in skeletal muscle, brain, or heart. In IL-10-deficient (IL-10 k/o) mice with no clinical or histological evidence of colitis, constitutive and TNF-alpha-induced expression of MAdCAM-1 in the intestine, cecum, and colon was not different from those values obtained with healthy wild-type controls. IL-10-deficient mice with active colitis exhibited a four- to fivefold greater expression of MAdCAM-1 in the cecum and colon compared with their healthy controls or to IL-10 k/o mice with no evidence of colitis. Taken together, these data demonstrate that TNF-alpha enhances surface expression of MAdCAM-1 in intestinal and colonic tissues to the same extent in both wild-type and IL-10 k/o mice with no colonic inflammation, whereas IL-10 k/o mice with active colitis exhibited a profound up-regulation of MAdCAM-1 in the colon.

Acute Disease↗
PubMed2001

SCFA increase intestinal Na absorption by induction of NHE3 in rat colon and human intestinal C2/bbe cells.

Short-chain fatty acids (SCFA), produced by colonic bacterial flora fermentation of dietary carbohydrates, promote colonic Na absorption through mechanisms not well understood. We hypothesized that SCFA promote increased expression of apical membrane Na/H exchange (NHE), serving as luminal physiological cues for regulating colonic Na absorptive capacity. Studies were performed in human colonic C2/bbe (C2) monolayers and in vivo. In C2 cells exposed to butyrate, acetate, proprionate, or the poorly metabolized SCFA isobutyrate, apical membrane NHE3 activity and protein expression increased in a time- and concentration-dependent manner, whereas no changes were observed for NHE2. In contrast, no significant changes in brush-border hydrolase or villin expression were noted. Analogous to the in vitro findings, rats fed the soluble fiber pectin exhibited a time-dependent increase in colonic NHE3, but not NHE2, protein, mRNA, and brush-border activity. These changes were region-specific, as no changes were observed in the ileum. We conclude that luminal SCFA are important physiological cues for regulating colonic Na absorptive function, allowing the colon to adapt to chronic changes in dietary carbohydrate and Na loads.

Animals↗
PubMed2005

Intestinal spirochetosis and colon diverticulosis.

A case of intestinal spirochetosis in a 62-year-old white male is reported. The condition was characterized by chronic flatulence and episodes of intestinal hemorrhage, in addition to the evidence of hypotonic diverticular disease, with a large number of slender organisms in the colon epithelium and cryptae. Spirochetes were demonstrated by Whartin-Starry stain. The serologic tests for syphilis and HIV were positive. Spirochetosis was treated with penicillin G, and the patient remains free of intestinal complaints 20 months later.

Anti-Bacterial Agents↗
PubMed1988

Susceptibility of germfree or antibiotic-treated adult mice to Cryptosporidium parvum.

Adult mice are more resistant than neonatal mice to intestinal colonization with the protozoan parasite Cryptosporidium parvum. Development of a mature intestinal flora may play a role in this resistance. We compared susceptibilities to colonization with C. parvum in adult conventional mice, adult germfree mice, and adult conventional mice treated with oral antibiotics to deplete the intestinal flora. Germfree mice of both CD1 and BALB/c strains were colonized at day 7 following inoculation with C. parvum oocysts isolated from the feces of an infected, diarrheic calf. Age-matched conventional mice of the same strains were comparatively resistant to colonization. Conventional mice treated with antibiotics remained resistant to colonization. These results suggest that the microflora in the intestine was not the sole determinant of resistance or susceptibility to colonization. The germfree adult mouse as an experimental model of cryptosporidiosis is discussed.

Animals↗
PubMed1992

Histological investigation of the myenteric plexus of the entire gut in an infant with hypogenesis of the intestine.

A male infant with pseudo-Hirschsprung's disease was treated for 2 years and 10 months, then died of severe enterocolitis. At autopsy examination of the entire gut was possible, and a definite histological examination could be performed which threw light on the pathogenesis. The ganglion cells of the esophagus, stomach, small intestine, colon and rectum were examined, diameters of their nuclei were measured, and their nuclear volumes were calculated. S-100 and anti-neurofilament stainings were also performed in an immunohistological investigation of the glial cells and nerve fibers. Both the diameter of the volume of the nuclei of the ganglion cells in the small intestine and colon were significantly smaller than normal. Even in the esophagus the nuclear volume was smaller than normal. The glial cells and nerve fibers gradually decreased in the caudal direction. Thus, histomorphometry and immunohistochemistry both showed that the neuroblasts in the intestine were immature and the migration of ganglion cells was disturbed in this case. The final diagnosis was hypogenesis of the intestine.

Cell Count↗
PubMed1999

Irradiation induces marked immunohistochemical expression of vasoactive intestinal peptide in colonic mucosa of man.

Vasoactive intestinal peptide (VIP) is known to modulate inflammatory reactions, to have trophic effects, and to contribute to diarrhea and has been implicated as an important factor in several inflammatory conditions in the human gut. The aim of the present study was to investigate the effects of irradiation on the expression of VIP in the colon of patients operated on for adenocarcinoma. Some of the patients had received preoperative irradiation (25 Gy) within one week before the operation. Specimens of sigmoideum, 10 cm cranial to the margin of the cancer, were examined, by using antiserum against VIP and immunohistochemistry. There were numerous nerve fibers showing VIP-like immunoreactivity in the damaged mucosa, including the regions showing ulcerations. There was a higher degree of expression of VIP in the ganglion cells in the submucous plexuses in irradiated than nonirradiated patients. The study shows that there is a marked immunohistochemical expression of VIP concomitant with the occurrence of inflammatory and repair processes in the irradiation-damaged human colonic mucosa.

Adenocarcinoma↗
PubMed2002

Novel genes and functional relationships in the adult mouse gastrointestinal tract identified by microarray analysis.

BACKGROUND & AIMS: A genome-level understanding of the molecular basis of segmental gene expression along the anterior-posterior (A-P) axis of the mammalian gastrointestinal (GI) tract is lacking. We hypothesized that functional patterning along the A-P axis of the GI tract could be defined at the molecular level by analyzing expression profiles of large numbers of genes. METHODS: Incyte GEM1 microarrays containing 8638 complementary DNAs (cDNAs) were used to define expression profiles in adult mouse stomach, duodenum, jejunum, ileum, cecum, proximal colon, and distal colon. Highly expressed cDNAs were classified based on segmental expression patterns and protein function. RESULTS: 571 cDNAs were expressed 2-fold higher than reference in at least 1 GI tissue. Most of these genes displayed sharp segmental expression boundaries, the majority of which were at anatomically defined locations. Boundaries were particularly striking for genes encoding proteins that function in intermediary metabolism, transport, and cell-cell communication. Genes with distinctive expression profiles were compared with mouse and human genomic sequence for promoter analysis and gene discovery. CONCLUSIONS: The anatomically defined organs of the GI tract (stomach, small intestine, colon) can be distinguished based on a genome-level analysis of gene expression profiles. However, distinctions between various regions of the small intestine and colon are much less striking. We have identified novel genes not previously known to be expressed in the adult GI tract. Identification of genes coordinately regulated along the A-P axis provides a basis for new insights and gene discovery relevant to GI development, differentiation, function, and disease.

Animals↗
PubMed1997

[Digestive hemorrhage disclosing an angiodysplasia and von Willebrand disease type 2].

The authors report a case of a 76-year-old man, with not past history of abnormal bleeding, who suffered an acute, recurrent, intestinal haemorrhage from extensive angiodysplasia of the colon. Intestinal bleeding and angiodysplasia were associated with a von Willebrand's disease. Genetic analysis showed a point mutation in arginine 611 of the mature von Willebrand's factor subunit (A1 loop) confirming a von Willebrand's disease type 2.

Aged↗
PubMed1977

Gastrointestinal myoelectrical activity in idiopathic intestinal pseudo-obstruction.

We evaluated the myoelectrical and motor function of the esophagus, small intestine, colon and anal sphincter in four patients with chronic idiopathic intestinal pseudo-obstruction. All patients had aperistalsis of the esophagus, with incomplete relaxation of the lower esophageal sphincter after swallowing or balloon distension. Duodenal slow-wave frequency was normal at 11.4+/-0.3 (+/-S.E.M.) cycles per minute. The patients did not have a normal increase in duodenal spike or motor activity after intestinal distension, but duodenal activity increased after stimulation with intravenous secretin. Colonic slow-wave activities were present at two frequencies, 6.2+/-0.3 and 3.3+/-0.1 cycles per minute. Neostigmine administration increased both colonic spike and motor activity normally. These studies suggest that in this disorder, physiologic neural responses to swallowing or intestinal distension are impaired but the intestinal smooth-muscle slow-wave activity and the spike and motor responses to exogenous neurohormonal stimulation are intact.

Adult↗
PubMed1990

Impaired colonization by and full invasiveness of Escherichia coli K1 bearing a site-directed mutation in the type 1 pilin gene.

A type 1 pilus-deficient mutant of a systemically invasive Escherichia coli K1 strain was constructed by directed mutagenesis of pilA, the gene that codes for the major structural subunit of type 1 pili. By comparing this mutant with an isogenic pilA+ strain, we were able to assess the role of type 1 piliation in alimentary tract colonization and bloodstream invasion in neonatal rats. Intestinal colonization was not significantly affected by the pilA mutation; in contrast, loss of type 1 piliation correlated with a dramatic decrease in oropharyngeal colonization. Nevertheless, development of bacteremia after oral administration of E. coli K1 was not diminished by the mutation in pilA. Thus, loss of type 1 piliation correlated with a site-dependent effect on colonization within the alimentary tract while not interfering with bloodstream invasion.

Animals↗
PubMed1989

Prospective survey of colonization and infection caused by expanded-spectrum-beta-lactamase-producing members of the family Enterobacteriaceae in an intensive care unit.

The occurrence of expanded-spectrum-beta-lactamase-producing strains was prospectively studied in 56 patients in an intensive care unit. Ten patients were infected or colonized; some of these patients had asymptomatic intestinal colonization. Four different expanded-spectrum beta-lactamases were identified and used as epidemiological markers to survey nosocomial infections.

Acute Kidney Injury↗
PubMed1988

Experimental infection of dogs with Campylobacter jejuni.

Three groups of conventional puppies were inoculated orally with Campylobacter jejuni biotype 2 which had been isolated from the small intestine of a dog with enteritis. Mild enteric disease was observed in one group. There was superficial intestinal colonization by the organism but penetration of intestinal epithelial cells was not apparent. C jejuni was isolated from the blood and viscera of inoculated dogs which showed no histological evidence of disease.

Animals↗
PubMed2000

[Amebiasis].

Amoebiasis caused by the enteric protozoan Entamoeba histolytica is a widespread parasitic disease, which causes 40,000 to 100,000 deaths per year. Cases diagnosed in Denmark are always imported. Infection results from ingestion of amoebic cysts, which after excystation form trophozoits in the small intestine, colonize the bowel lumen and invade the intestinal epithelium resulting in amoebic colitis. Spread to the liver and formation of amoebic liver abscesses occurs in one third of the cases, whereas other extraintestinal manifestations are rare. Amoebic colitis and liver abscess have a good prognosis when treated with metronidazole, whereas complications such as necrotizing colitis, peritonitis and pericarditis have a high mortality. An early diagnosis and treatment is therefore important. Intestinal amoebiasis is diagnosed by demonstration of E. histolytica cysts or amoebae in the stools, whereas serology is of value in diagnosing extraintestinal amoebiasis in nonendemic regions.

Animals↗
PubMed2001

Apomucin expression and association with Lewis antigens during gastric development.

In normal stomach, MUC5AC and MUC6 apomucins are associated with Lewis types 1 and 2, respectively, and this association is lost during gastric carcinogenesis. The expression of gastric (MUC5AC, MUC6) and intestinal (MUC2, MUC4) apomucins and Lewis antigens during gastric development, using single and double labeling immunohistochemistry on fetal tissues (15-41 weeks), was analyzed and related to the tumor expression patterns. Apomucin expression in other fetal tissues was also analyzed. In gastric samples, MUC2 is detected in 14 of 19 showing no correlation with fetal age, and MUC4 is not detected. MUC5AC and MUC6 are always highly detected and are coexpressed and associated with both types of Lewis antigens. These patterns change progressively with the development of the adult gastric morphology. MUC2 is detected in the small intestine, colon, and pancreas; MUC4 is expressed in the colon; MUC5AC is detected in the small intestine; and MUC6 is found in the duodenum and pancreas. The patterns of apomucin expression and association with Lewis antigens during development are complex, but there is a trend toward the establishment of the adult pattern, with the exception of MUC4, which is not detected. These patterns found in fetal stomach indicate that alterations reported in gastric tumors do not fully recapitulate a developmental phenotype.

Digestive System↗
PubMed1991

Effect of glucose treatment on carbohydrate content in various organs in mice after acute As2O3 poisoning.

Glucose treatment improved survival and symptoms in mice poisoned with As2O3. In order to get more insight into the mechanisms involved, postmortum changes in glucose and glycogen content of various organs and pathology were investigated in mice acutely poisoned with As2O3 and treated with glucose. Forty mice each received 12.9 mg As2O3/kg sc as a single injection. The first group of 10 mice had no further treatment. Fifteen minutes after the As2O3 injection and every 2 h thereafter, the second group (10 mice) received saline and the third group (10 mice) received 5% glucose ip. Groups 4 and 5 (5 mice each) received either saline or glucose only. The injection volume in all groups was 10 microliters/g mouse. Group 6 (5 mice) had no treatment whatsoever. Immediately after death brain, muscle and kidneys were prepared for the enzymatic determination of glucose and glycogen. Samples of the brain, muscle, kidneys, liver, small intestine, colon and spleen were taken for microscopic examination. Independent of the therapeutic procedure, decreases in the glycogen in livers and increases in fat in livers and muscles were observed in mice which died. All mice which died showed heavy leucocytes disruptions, increased fat, and decreased glycogen in the spleen. Intrafolliculary disruptions of leucocytes in the small intestine and colon, as well as patchy hyperemias and hemorrhagic spots in the papilla of the kidneys, were observed in non-survivor mice. Decreased glucose and glycogen was in the brains of non-survivor mice; no differences in glucose and glycogen were found in brains of the mice which survived.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1990

[Effects of a new derivative of 5-alkyl-3N-furanones on the colonization resistance of the intestine in albino mice].

By its antagonistic function normal microflora provides the intestine with resistance to colonization with exogenic opportunistic and pathogenic microorganisms. The drug was effective in inducing a decrease in the intestine colonization resistance which in its turn leads to filling of free ecological niches with exogenic microflora. In this connection the suggestion that specification of a new chemical agent should include along with other criteria its effect on colonization resistance is valid. It was shown with the use of indicator microorganisms that when administered per os in doses of 40 and 80 mg/kg daily for 3 and 6 days, respectively, a new original compound 1929, a derivative of 5-alkyl-3H-furanones, with high antimicrobial activity induced no significant or more pronounced changes in the colonization resistance of the gastrointestinal tract of noninbred albino mice than furagin used as the reference drug.

Animals↗
PubMed1997

Inhibition of 5'-deoxy-5-fluorouridine phosphorolysis by acyclothymidine in tumor cell homogenates.

The inhibitory effect of acyclothymidine[AcyT, 5-methyl-1-(2'-hydroxyethoxymethyl) uracil], a potent pyrimidine nucleoside phosphorylase (PyNPase) inhibitor, on 5'-deoxy-5-fluorouridine (5'-DFUR) phosphorolysis in human and mouse tumor cell homogenates was measured. Competitive inhibition was observed in MKN-74 and Lewis lung carcinoma (LLC), whereas non-competitive inhibition was observed in HeLa. The strength of the inhibitory effect by AcyT showed the following pattern: HeLa < human normal intestine < mouse normal intestine < Colon 26 < LLC < MKN-74 < DLD-1. From the kinetic parameter obtained, we simulated the inhibitory effect of AcyT on 5'-DFUR phosphorolysis in tumor cells and the intestine. These data indicated that AcyT was more sensitive in normal mouse intestine than in Colon 26 and LLC, and that orally administered AcyT can reduce the intestinal toxicity of 5'-DFUR without reducing the antitumor effect in the mouse. The present finding may have an important implication for attempts to introduce AcyT, a potent PyNPase inhibitor, into the clinic.

Animals↗
PubMed2004

Identification of one exon deletion of intestinal alkaline sphingomyelinase in colon cancer HT-29 cells and a differentiation-related expression of the wild-type enzyme in Caco-2 cells.

Sphingomyelin (SM) metabolism in the gut has been implicated in colonic tumorigenesis. Intestinal alkaline sphingomyelinase (alk-SMase) hydrolyses SM in the intestinal content and at the brush border. The enzyme activity is decreased in the tissues of human colorectal tumours. This study examines whether site or chain-mutation of alk-SMase occurs in colon cancer HT-29 cells and Caco-2 cells. Total RNA was isolated and the cDNA of alk-SMase was amplified by RT-PCR. The size of the cDNA from HT-29 cells was smaller than that of the wild-type cDNA. DNA sequencing identified a deletion of exon 4 in alk-SMase cDNA in HT-29 cells. No mutation in genomic alk-SMase DNA from exon 3 to 5 was identified. The exon 4 deletion was caused by a shift of RNA splice site in chromosome 17q25. In Caco-2 cells, no mutation of alk-SMase cDNA was identified. Transient expression in COS-7 cells showed that the enzyme from the cDNA in HT-29 cells had little alk-SMase activity whereas that in Caco-2 cells was as active as the wild-type alk-SMase. The deleted region included residue His353, which is predicted to form a substrate-binding site of alk-SMase. H353A substitution resulted in a protein with no alk-SMase activity. In monolayer cultured Caco-2 cells and HT-29 cells the alk-SMase activities were low. However, to culture the cells under polarizing conditions increased alk-SMase activity and reduced SM level in Caco-2 cells. The alk-SMase activity varied in parallel with alkaline phosphatase activity. In conclusion, we identified an inactive deletion in alk-SMase in HT-29 cells, and a differentiation-related expression of the enzyme in Caco-2 cells. The results provide a molecular mechanism related to previous findings of reduced alk-SMase activity in human colon cancers.

Alkaline Phosphatase↗