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PubMed1985

Physiology of the splanchnic circulation.

The splanchnic circulation is composed of gastric, small intestinal, colonic, pancreatic, hepatic, and splenic circulations, arranged in parallel with one another. The three major arteries that supply the splanchnic organs, cellac and superior and inferior mesenteric, give rise to smaller arteries that anastomose extensively. The circulation of some splanchnic organs is complicated by the existence of an intramural circulation. Redistribution of total blood flow between intramural vascular circuits may be as important as total blood flow. Numerous extrinsic and intrinsic factors influence the splanchnic circulation. Extrinsic factors include general hemodynamic conditions of the cardiovascular system, autonomic nervous system, and circulating neurohumoral agents. Intrinsic mechanisms include special properties of the vasculature, local metabolites, intrinsic nerves, paracrine substances, and local hormones. The existence of a multiplicity of regulatory mechanisms provides overlapping controls and restricts radical changes in tissue perfusion.

Colon↗
PubMed1998

Apical secretion of a pathogen-elicited epithelial chemoattractant activity in response to surface colonization of intestinal epithelia by Salmonella typhimurium.

Modeling Salmonella-epithelial cell interaction in vitro has led to the realization that epithelial cells are crucial in orchestrating neutrophil (PMN) responses, in part by stimulating basolateral release of epithelial chemokines, including IL-8. However, such basolaterally released chemokines, while likely important in orchestration of PMN movement across the subepithelial matrix, are unlikely to be responsible for the final step of transepithelial migration of PMN and entry into the apical compartment. We now show that S. typhimurium attachment to T84 cell apical epithelial membranes induces polarized apical secretion of a pathogen-elicited epithelial chemoattractant (PEEC) bioactivity. Experiments employing semipurified PEEC indicate that it is released in a polarized apical fashion and is sufficient to explain the observed final step of transepithelial migration of PMN induced by Salmonella-apical membrane interaction. By preliminary physical characterization and profiles of PMN activation, PEEC appears to be a novel PMN chemotactic bioactivity. This 1- to 3-kDa nominal molecular mass chemokine-like bioactivity directly stimulates PMN via a pertussis toxin-sensitive receptor and elicits a Ca2+ signal. While these latter features are shared by most other chemokines, analysis of PEEC-elicited PMN activation reveals that, unlike these other agonists, PEEC, even at saturating concentrations, elicits chemotactic activity in the absence of stimulation of superoxide production and/or release of primary and/or secondary granules. These data suggest that the apically released PEEC activity appears to represent a novel epithelial-derived chemoattractant that directs PMN movement across epithelial monolayers.

Antigens, CD↗
PubMedDate not supplied

[Digestive and cutaneous colonization of Staphylococcus aureus, Pseudomonas aeruginosa and Corynebacterium xerosis in germ-free hairless mice].

Regardless of the method of germ-free HRS mouse contamination, the kinetics of Staphylococcus aureus and Pseudomonas aeruginosa cutaneous colonization was parallel to the kinetics of intestinal colonization; Corynebacterium xerosis, however, was unable to colonize the skin or the gastrointestinal tract. There was little variability in intestinal and cutaneous colonization; this was quite different from observations in man and hairless holoxenic mice. It is possible to use these experimental models to standardize the measurement of antiseptic bactericidal activity in vivo.

Animals↗
PubMed2002

CDX2 regulates liver intestine-cadherin expression in normal and malignant colon epithelium and intestinal metaplasia.

BACKGROUND & AIMS: The intestine-specific caudal-related homeobox transcription factor CDX2 seems to play a key role in intestinal development and differentiation. Inactivation of one Cdx2 allele predisposes mice to develop colon polyps, and loss of CDX2 expression is a feature of some poorly differentiated colon carcinomas in humans. Conversely, aberrant CDX2 expression is often seen in intestinal metaplasias in the stomach and esophagus and in some gastric carcinomas. To better understand CDX2 function, we sought to define CDX2-regulated genes. METHODS: HT-29 colon cancer cells with minimal endogenous CDX2 expression were engineered to express exogenous CDX2, and gene expression changes relative to control cells were assessed using high-density oligonucleotide arrays. RESULTS: The gene for liver intestine (LI)-cadherin (cadherin 17) was strongly induced by CDX2 in HT-29. In other colorectal cancer lines, endogenous CDX2 and LI-cadherin expression were well correlated. Activation of a ligand-regulated form of CDX2 rapidly induced LI-cadherin gene expression, even in the presence of protein synthesis inhibitor. Analysis of the 5'-flanking region of the LI-cadherin gene defined 2 CDX2 responsive elements, and chromatin immunoprecipitation assays indicate CDX2 binds to the elements. In primary colorectal cancers and intestinal metaplasias in the stomach, CDX2 and LI-cadherin expression were tightly correlated. CONCLUSIONS: CDX2 regulates LI-cadherin gene expression in normal, metaplastic, and neoplastic tissues of the gastrointestinal tract via binding to elements in the 5'-flanking region of the gene. Given the well-established roles of cadherins in morphogenesis and differentiation, LI-cadherin may be a key factor mediating CDX2 function in intestinal cell fate determination.

Animals↗
PubMed2002

Evolutionary and functional analyses of variants of the toxin-coregulated pilus protein TcpA from toxigenic Vibrio cholerae non-O1/non-O139 serogroup isolates.

The toxin-coregulated pilus (TCP) is a critical determinant of the pathogenicity of Vibrio cholerae. This bundle-forming pilus is an essential intestinal colonization factor and also serves as a receptor for CTXphi, the filamentous phage that encodes cholera toxin (CT). TCP is a polymer of repeating subunits of the major pilin protein TcpA and tcpA is found within the Vibrio pathogenicity island (VPI). In this study genetic variation at the tcpA locus in toxigenic isolates of V. cholerae was investigated and three novel TcpA sequences from V. cholerae strains V46, V52 and V54, belonging to serogroups O141, O37 and O8, respectively, were identified. These novel tcpA alleles grouped into three distinct clonal lineages. The polymorphisms in TcpA were predominantly located in the carboxyl region of TcpA in surface-exposed regions of TCP fibres. Comparison of the genetic diversity among V. cholerae isolates at the tcpA locus with that of aldA, another locus within the VPI, and mdh, a chromosomal locus, revealed that tcpA sequences are far more diverse than these other loci. Most likely, this diversity is a reflection of diversifying selection in adaptation to the host immune response or to CTXphi susceptibility. An assessment of the functional properties of the variant tcpA sequences in the non-O1 V. cholerae strains was carried out by analysing whether these strains could be infected by CTXphi and colonize the suckling mouse. Similar to El Tor strains of V. cholerae O1, in vitro CTXphi infection of these strains required the exogenous expression of toxT, suggesting that in these strains ToxT regulates TCP expression and that these TcpA variants can serve as CTXphi receptors. All the V. cholerae non-O1 serogroup isolates tested were capable of colonizing the suckling mouse small intestine, suggesting that the different TcpA variants could function as colonization factors.

Alleles↗
PubMed1982

Colonic and small intestinal alkaline phosphatase. A histochemical and biochemical study.

Colonic and intestinal alkaline phosphatase were studied histoenzymatically and biochemically in normal mucosae from eight hemicolectomy specimens. Histochemically, the most intense reaction was found in the small intestine, followed by vascular endothelium and colonic epithelium, respectively. The reaction was stronger in frozen sections than in acetone-fixed specimens, weakest in formalin-fixed tissues, and best when cold fixatives and low melting point paraffin were used. In the small intestine, the reaction was most marked on the villus tips. In the colon, the crypt necks showed the strongest reaction although good staining of luminal epithelium was found with more prolonged incubation. The addition of phenylalanine to the substrate medium resulted in selective inhibition of epithelial staining, whereas levamisole selectively inhibited the vascular reaction. On cellulose acetate electrophoresis, colonic and intestinal alkaline phosphatase showed slightly different rates of migration suggesting the presence of different isoenzymes. Quantitative analysis indicated that the intestinal enzyme expressed in U/g wet tissue was 7.7 times the colonic enzyme in amount. It is concluded that despite its relatively low biochemical activity, alkaline phosphatase can be demonstrated histochemically in colonic epithelium if tissues are processed at low temperatures and if the appropriate fixatives and adequate times are used.

Alkaline Phosphatase↗
PubMed1991

Long-term effect of Bifidobacteria and Neosugar on precursor lesions of colonic cancer in CF1 mice.

This investigation was undertaken to study the role of Bifidobacteria and bifidogenic factor Neosugar in the process of 1,2-dimethylhydrazine-induced colonic carcinogenesis in CF1 mice. Intestinal colonization and selective proliferation of Bifidobacteria were achieved by oral administration of indigenous Bifidobacteria and the incorporation of 5% Neosugar in the diet of animals. The Bifidobacteria were isolated from the feces of CF1 mice and were identified to be Bifidobacterium pseudolongum biovar b. This incidence of aberrant crypts and foci were significantly lower 38 weeks after the last injection of the carcinogen in animals fed Bifidobacteria than in animals treated with the carcinogen alone. The aberrance also appeared to be confined to the more distal end of the colon in animals fed bifidogenic diet. Such changes in the precursor lesions of colonic carcinogenesis are presumably due to the increase in the number of Bifidobacteria and their acidifying action in the lower intestinal tract of the animals.

Animals↗