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1-Naphthol beta-D-glucuronide formed intraluminally in rat small intestine mucosa and absorbed into the colon.

UDP-glucuronosyltransferase expressed in the rat intestinal epithelial cells is important as the first barrier against chemicals. The distribution of 1-naphthol and its glucuronide formed in rat intestine was estimated by using everted intestine. Roughly 60% of the 1-naphthol added to the mucosal fluid was absorbed into the mucosa of the small intestine and colon within 30 min. Approximately 66% of the 1-naphthol absorbed in the proximal intestine was secreted intraluminally as a glucuronide, and a minimal 9% was transported into the serosal fluid as a glucuronide. In the distal intestine, approximately 34% was secreted intraluminally and 30% was transported into the serosal fluid as a glucuronide. The greatest amount of the glucuronide (37% of the absorbed 1-naphthol) was transported into the serosal fluid, whereas a minimal 7% was secreted intraluminally in the colon. In marked contrast, the colon was found to transport 1-naphthol-glucuronide from the mucosal fluid into the serosal fluid at an approximately 8-fold higher rate than that of the small intestine. These results suggest that, in the small intestine, phenolic xenobiotics are mostly glucuronidated and secreted intraluminally and that the resulting glucuronide is absorbed and transported into the serosal side of the colon.

Animals↗

Herbicide/pesticide effects on intestinal epithelial growth.

The purpose of the present study was to examine the effects of some common herbicides and pesticides on the growth of normal intestinal and colonic epithelial cells. Preconfluent cultures of normal rat intestinal cells (IEC-6 cell line) and normal human colonic epithelial cells were treated with 0.05-50 microM doses of atrazine, diazinon, and endosulfan. After 3 days of treatment, the change in cell proliferation was quantified by cell counting or the MTT growth assay. Both intestinal and colonic epithelial cell cultures had increases in cell growth when treated with as little as 1.0 microM atrazine, diazinon, or endosulfan. The observed changes in both cultured intestinal and colonic cell growth rates were not due to the influence of the vehicle control dimethyl sulfoxide (DMSO). That is, the treatment of the cell cultures with concentrations of DMSO as high as 0.5% for 3 days resulted in no change in cell growth compared with untreated control cultures. A consistent observation with all three of the compounds was that the highest doses (50 microM) had the least "proliferative potential" in stimulating either IEC-6 cell or human colonic epithelial cell growth. Within the concentration range used, none of the herbicides or pesticides caused a decrease in cell proliferation below that of the untreated control cultures. Overall, treatment of IEC-6 cell cultures with atrazine, diazinon, or endosulfan produced a biphasic growth response, whereas the same treatment in the human colonic epithelial cell cultures produced a more sustained level of growth over the same period. This culture system may provide the basis for an in vitro model to further study the cellular and molecular basis of the effects of herbicides and pesticides on intestinal epithelial proliferation.

Animals↗

Tenascin expression in relation to stromal tumour cells in canine gastrointestinal epithelial tumours.

The expression of tenascin, alpha-smooth muscle actin (alpha-SMA), desmin and vimentin was investigated immunohistochemically in the stroma of normal canine stomach, small intestine and colon, and in 30 epithelial tumours of the canine stomach, small intestine or colon. In addition, "co-localization" of tenascin and alpha-SMA was investigated by double immunohistochemistry. Tenascin was absent in the normal gastric mucosa but present in the normal intestine, with a gradual increase in immunolabelling intensity from the cryptal glands to the surface epithelium. Tenascin expression was greater in all adenomas and carcinomas than in normal tissues. Two different patterns of tenascin expression were observed in all carcinomas, irrespective of their site. In well-differentiated tumour regions of both gastric and intestinal tumours, a fibrillary sub-glandular expression was observed; in poorly differentiated tumour regions, however, the expression pattern was diffuse. Incomplete invasion of the muscularis mucosae was accompanied by thickening and increased tenascin expression. In normal stomach and intestines, alpha-SMA and desmin were demonstrated in pericryptal myofibroblasts and smooth muscle cells of the muscle layers. In colonic adenomas and gastric and intestinal carcinomas, alpha-SMA was demonstrated in all stromal cells surrounding tumour cells. In contrast to alpha-SMA labelling, desmin labelling was negative in tumour stromal cells (in both gastric and intestinal tumours), except in tumour regions close to the muscularis mucosae. This suggested that myofibroblasts in gastric and intestinal tumours originated from pre-existing fibroblasts, except in tumour regions close to the muscularis mucosae, where the myofibroblasts seemed to originate from smooth muscle cells of the muscularis mucosae. There was a strong co-localization of tenascin and alpha-SMA-expressing myofibroblasts, suggesting that myofibroblasts are responsible for tenascin secretion.

Adenocarcinoma↗

Characterization and autoradiographic localization of multiple tachykinin binding sites in gastrointestinal tract and bladder.

Binding sites for the [125I]Bolton-Hunter-labeled tachykinins substance K (BHSK), eledoisin (BHE) and substance P (BHSP) were investigated using crude membrane suspensions and autoradiography. In smooth muscle membranes from guinea-pig small intestine and rat duodenum, specific binding of BHSK was saturable and reversible, showing a single class of sites with a KD of 1 to 3 nM and maximum number of specific binding sites of 1 to 2 fmol/mg of wet weight tissue. Pharmacological characterization of this binding revealed a novel receptor site (K) with affinity for substance K greater than kassinin greater than or equal to eledoisin greater than neuromedin K greater than substance P greater than physalaemin. Inhibition of the binding of BHSK in membranes from mouse urinary bladder exhibited a similar K-type pattern. In rat duodenum and mouse bladder membranes, the binding of BHE was inhibited by substance K greater than kassinin greater than eledoisin greater than neuromedin K greater than substance P greater than physalaemin indicating the same receptor site as for BHSK. On the other hand, in rat cerebral cortex membranes BHE binding was inhibited by neuromedin K = kassinin = eledoisin greater than physalaemin greater than substance K greater than substance P indicating a definitive tachykinin E receptor site. The same displacement pattern of BHE binding was also detected in longitudinal muscle membranes from the guinea-pig small intestine. In mouse bladder membranes and in rat and guinea-pig intestine, the binding of BHSP was inhibited by substance P greater than physalaemin greater than substance K greater than or equal to eledoisin = kassinin greater than neuromedin K indicating a definitive tachykinin P receptor site. Autoradiographic binding sites for both BHSK and BHSP were seen in circular muscle of the rat stomach, small intestine and colon and in circular and longitudinal muscle of the guinea-pig small intestine and colon. Binding sites for BHSK, but not for BHSP, were seen in the muscularis mucosae of the gastric fundus and colon of the rat. Binding sites for BHSP, but not for BHSK, were seen in mucosa of guinea-pig colon and were densely clustered over ganglia of the myenteric and submucous plexuses in rat and guinea-pig colon. The guinea-pig intestine probably contains all three types of tachykinin binding sites whereas rat duodenum and mouse bladder contain only K and P sites. Some tissues classified previously as SP-P or SP-E may actually contain P and/or K sites.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Amounts of intestinal microflorae in relation to colon carcinogenesis. An experimental study.

Quantitative analysis of intestinal microflorae in the diverted and feces-containing portions of the colon after performing an ascendo-descendostomy Roux en Y in Wistar-Lewis rats, the colonic portion from the ascending colon to the midportion of the descending colon being diverted from the fecal stream, disclosed a drastic decrease in the total amount of the intestinal microflora as well as most anaerobic microflorae in the diverted portion of the colon where the amount of the colonic content was extremely reduced. This diverted segment was least susceptible of developing macroscopical epithelial neoplasia after exposure to a carcinogen, MNNG, sufficient in amount to evoke multiple large neoplasia in the ordinary colon, although microscopical intramucosal neoplastic foci were induced there. Thus the existence of the intestinal content was essential for the process of promotion in experimental colonic carcinogenesis. The close parallelism between amounts of intestinal content and amounts of intestinal microflorae, especially anaerobic ones, suggested the roles of anaerobic microflorae in colonic carcinogenesis.

Anaerobiosis↗

Immunohistological characterization of intraepithelial and lamina propria lymphocytes in control ileum and colon and in inflammatory bowel disease.

Using monoclonal antibodies to T and B lymphocytes, to natural killer cells, and to HLA-DR antigen, we characterized the lymphocyte population within the epithelial and lamina propria regions in control intestine and colon, and in grossly involved and in grossly uninvolved intestine and colon of patients with active inflammatory bowel disease. There were significantly more intraepithelial T cells in control ileum than in control colon. In comparison to control, there was a heterogeneity of alterations in intraepithelial and lamina propria T lymphocyte subsets (T11+, T8+, T4+) in inflammatory bowel disease. B lymphocytes were not detected within the lamina propria, except when found in and adjacent to lymphoid aggregates. Leu 7+ cells were uncommon in the lamina propria of control ileum and colon and in diseased tissues. The majority of intraepithelial lymphocytes did not express HLA-DR. Epithelial cells of control colon did not express HLA-DR while epithelial cells of control ileal tissues and of diseased colonic and ileal specimens expressed HLA-DR antigen. Only small numbers of lamina propria T cells expressed HLA-DR in both control and disease tissues. There was intense expression of HLA-DR by monocytes and modest expression of HLA-DR by capillary and lymphatic endothelial cells. The induction of HLA-DR expression by diseased colonic epithelium and the observation that lymphatic endothelium expresses HLA-DR are new observations, and we established that Leu 7+ cells are present in very small numbers in both normal and diseased intestine and colon.

Antibodies, Monoclonal↗

[Recurrent sanguineous and mucous diarrhea and spasms in a 46-year-old woman--manifestation of endometriosis in the colon sigmoideum].

Intestinal endometriosis is the most frequent extragenital manifestation of this disease. Sometimes patients even present with acute bowel obstruction. We report on a 46-year-old woman complaining about recurrent sanguineous and mucous diarrhea and spasms for several years. Colonoscopy showed a stenosis in the sigmoid colon without macroscopically visible alterations of the mucosa. Computertomography, ultrasound and barium contrast enema did not provide us with further information about the origin of the stenosis. Biopsies out of the mucosa at the stenosis showed typical endometriosis tissue. After starting a conservative therapy with GnRH-agonist gosereline the patient became completely free of symptoms. The coincidence of endometriosis and M. Crohn has to be taken into consideration. Therapy planning should include a close co-operation with gynaecologists and surgeons to transfer the patient to surgical intervention when needed.

Colon, Sigmoid↗

Identification of Escherichia coli O157 : H7 genes influencing colonization of the bovine gastrointestinal tract using signature-tagged mutagenesis.

Enterohaemorrhagic Escherichia coli (EHEC) cause acute gastroenteritis in humans that may be complicated by life-threatening systemic sequelae. The predominant EHEC serotype affecting humans in the UK and North America is O157 : H7 and infections are frequently associated with contact with ruminant faeces. Strategies to reduce the carriage of EHEC in ruminants are expected to lower the incidence of human EHEC infections; however, the molecular mechanisms underlying persistence of EHEC in ruminants are poorly understood. This paper reports the first comprehensive survey for EHEC factors mediating colonization of the bovine intestines by using signature-tagged transposon mutagenesis. Seventy-nine E. coli O157 : H7 mutants impaired in their ability to colonize calves were isolated and 59 different genes required for intestinal colonization were identified by cloning and sequencing of the transposon insertion sites. Thirteen transposon insertions were clustered in the locus of enterocyte effacement (LEE), which encodes a type III protein secretion system required for the formation of attaching and effacing lesions on intestinal epithelia. A putative structural component of the apparatus (EscN) is essential for intestinal colonization; however, the type III secreted effector protein Map plays only a minor role. Other Type III secretion-associated genes were implicated in colonization of calves by E. coli O157 : H7, including z0990 (ecs0850), which encodes the non-LEE-encoded type III secreted effector NleD and the closely related z3023 (ecs2672) and z3026 (ecs2674) genes which encode homologues of Shigella IpaH proteins. We also identified a novel fimbrial locus required for intestinal colonization in calves by E. coli O157 : H7 (z2199-z2206; ecs2114-ecs2107/locus 8) and demonstrated that a mutant harbouring a deletion of the putative major fimbrial subunit gene is rapidly out-competed by the parent strain in co-infection studies. Our data provide valuable new information for the development of intervention strategies.

Animals↗

[A contribution to congenital segmental intestinal dilatation (author's transl)].

Segmental intestinal dilatation is rare and has so far been described for 26 patients only. The article presents three own observations. The clinical symptoms correspond to those of intestinal obstruction and are in most cases manifest in infancy and early childhood. The affected section of the intestine is dilated regionally to 3 to 4 times the normal value and can be situated both in the small intestine and in the colon. The intestinal wall is thickened or thinned; all intestinal wall layers are preserved and the ganglionic cells are regular. A characteristic feature is the histological finding of heterotopic tissue such as gastric mucosa and tissue of pancreas, lung or cartilage. The mesenterial veins are markedly congested. In 50% of all patients association with other malformations is seen.

Abnormalities, Multiple↗

[Lactose intolerance in chronic inflammatory bowel diseases].

In 124 patients with Crohn's disease (69 women, 55 men; mean age 33.7 [11-66] years) and 53 with ulcerative colitis (30 women, 23 men; mean age 36.2 [19-74] years) the incidence of lactose intolerance, as measured by the H2 breath test and blood sugar concentration, was determined prospectively. To exclude abnormal bacterial colonization of the small intestine or rapid small-intestine transit after partial resection of the small intestine as a cause of lactose intolerance, the oro-caecal transit time for lactulose (H2 breath test) was measured. While 21 of 124 patients with Crohn's disease (16.9%) had the expected incidence of lactose intolerance, this was present in only 2 of 53 patients with ulcerative colitis (3.8%; P < 0.05). The lactose intolerance was independent of the site of any inflammatory changes, disease activity and extent of small-intestine resection. Oro-caecal transit time for lactose was similar for all patients. There was no lactose intolerance in two patients with abnormal small-intestinal bacterial colonization.--Because of their considerable diagnostic and prognostic significance, tests for lactose intolerance should be performed routinely in all cases of Crohn's disease or ulcerative colitis.

Adolescent↗

Intestinal ischemic disorders.

The physiology of the mesenteric circulation is described emphasizing important aspects of microcirculatory function and the factors which regulate blood flow to the bowel. Next, the pathophysiology of intestinal ischemia is considered with special focus on the disturbed mechanisms involved in ischemic disorders, such as active oxidant formation and inhibition of intrinsic protective systems. The histopathology of small intestinal and colonic ischemia and infarction is described. Finally, clinical issues are addressed including the diagnostic challenge and the management of these life-threatening disorders.

Colon↗

[Endogenous reinfection as a cause of recurrent genital candidiasis on women].

The cause of primary, recurrent genital candidosis (RGC), that 5% of the female population was afflicted with, is still unknown. It is not clear whether RGC is a result of reinfection or infection recidive caused by Candida sp. The goal of the study is to examine Candida presence in women's genital and intestinal tract; by resistotypization of the same isolated species of Candida fungi to prove their identity as well as the validity of the stated thesis that endogenous reinfection may be one of the possible causes of RGC. The study included 70 women (T-group) afflicted with primary RGC who, at the moment of the examination, were in the phase of manifest infection. In the control group there were 70 women (C-group) not afflicted with RGC. The microbiological test consisted of the microscopic and culture examination of women's genital and intestinal material. The Candida species were differentiated according to the gemination test and the biochemical activity measured by commercial Candi-Fast-test (Mycoplasma International, France) and Vitec-AMS-system (bioMerieux, France). Candi-Fast test examined the sensitivity of Candida species to antimicotics and determined the resistotypes of isolated species. The study did not show statistically significant difference between examined groups in terms of the Candida presence in intestinal tract. The Candida colonization of intestinal mucosa was proved in 24 women (34.28%) with RGC. Eighteen women (25.71%) of the control group, had Candida sp. in intestinal tract. The most frequent RGC agent, as well as most frequent coloniser of intestinal mucosa is Candida albicans (C. albicans--RGC--84.28%; T-group--intestinal tract--C. albicans--87.50%; C-group--intestinal tract--C. albicans--94.44%). In 20 women with RGC there was a presence of identical resistotypes of isolated Candida sp. Identical resistotypes of C. albicans was found in 19 women of the test group, in their genital and intestinal tract. Only in one patient it was recorded the same resistance types of C. trapicalis. In four patients Candida species isolated from genital and intestinal material were not identical. In two women with RGC C. albicans on vaginal mucosa was accompanied by C. glabrata in intestinal tract, while in two more women the presence of various resistotypes C. albicans was identified in genital and intestinal tract.

Adult↗

[Modifications of gastric mucosa in diffuse and intestinal cancer].

The study was made of 29 intestinal type gastric carcinomas, 37 diffuse type gastric carcinomas and stomach mucosa (SM). Both carcinomas slightly differed by frequency of the fundal glands atrophy. Intestinal type was characterized by a higher frequency of antral glands atrophy, intestinal metaplasia, particularly of colon type. Intestinal cell differentiation was about the same in both types. Hyperplasia of lining and endocrine cells in the fundal part of the mucosa was more frequent and neuroendocrine differentiation was more pronounced in diffuse stomach carcinoma. It is suggested that environmental impacts including helicobacter pylori result in proliferation of the epithelium, intestinal metaplasia, dysplasia and carcinoma of the intestinal type. Diffuse carcinoma is associated with proliferation of glandular epithelium (parietal, endocrine, cervical) due to genetic factors, hypergastrinemia caused by fundal gland atrophy, alkalization of the mucosa due to Helicobacter pylori infection.

Adenocarcinoma↗

[Bacterial-fungal associations in the intestine under the conditions of colonization by yeast-like fungi of the genus Candida].

The composition of the fecal microflora in somatic patients and patients with enteric infections under the conditions of surpluscolonization by yeast-like fungi of the genus Candida was analyzed. The study revealed that the high level of fungal contamination was linked with decreased colonization resistance of the intestine (deficiency in bifidoflora) and with the presence of opportunistic microorganisms: Staphylococcus aureus, hemolytic and lactose-negative Escherichia coli, as well as nonfermenting Gram negative bacteria. The antilysozyme activity of enterobacteria was found to increase in the course of their joint cultivation with fungi of the genus Candida, that may be regarded as one of the mechanisms of the formation and maintenance of pathobiocenosis.

Bacteria↗