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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risk of colorectal carcinoma is increased among patients with longstanding ulcerative colitis and Crohn's disease. The development of cancer in inflammatory bowel disease is hypothesized to evolve by a multistep process involving genetic instability, clonal expansion and the development of a malignant phenotype. The contribution of nutritional factors such as folate deficiency is of great interest; molecular genetic mechanisms are under study. In contrast to sporadic colorectal carcinoma, carcinomas in ulcerative colitis are associated with a long prior history of chronic inflammation and the subsequent development of epithelial dysplasia. Dysplasia is defined as an unequivocal neoplastic alteration of the colonic mucosa. The object of surveillance is prevention of death from cancer by detection at a premalignant or early curable stage. Patients at greatest risk of cancer who customarily undergo endoscopic surveillance are those with extensive colitis of more than 8 years duration. Dysplastic epithelium may occur in flat mucosa, and may produce a plaque or a nodular/villiform appearance. Dysplasia is not present in all patients with cancer in colitis. It is important to develop more sensitive and specific markers for the presence of precancer or cancer in colitis. Under study are proliferation-associated markers detected by immunohistochemistry, lectin binding, flow cytometry and laser-induced fluorescence coupled with endoscopy.
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PMID:Ulcerative colitis and colon cancer: biology and surveillance. 146 4

Entamoeba histolytica infection results in either asymptomatic colonization or invasive colitis and liver abscess. E. histolytica isolates from patients with invasive disease have characteristic isoenzyme profiles (pathogenic zymodemes), suggesting a role for parasite factors in determining the severity of infection. A galactose-specific cell surface lectin from a pathogenic zymodeme was shown to mediate in vitro adherence to human colonic mucins and contact-dependent killing of target cells. Six nonoverlapping antigenic determinants were identified on the 170-kilodalton heavy subunit of the pathogenic lectin. Anti-lectin monoclonal antibodies (MAb) directed against epitopes 1 and 2 enhanced adherence whereas MAb to epitopes 3 through 6 either inhibited or had no effect on adherence. We tested 50 pathogenic and nonpathogenic strains for reactivity to these anti-lectin MAb by radioimmunoassay. MAb to epitopes 1 through 6 reacted in the radioimmunoassay with all 16 pathogenic zymodeme strains tested. In contrast, only MAb to epitopes 1 and 2 bound to the lectin from nonpathogenic strains. Western immunoblots with anti-lectin antibodies showed that the 170-kilodalton heavy subunit was present in the nonpathogenic amebae. Adherence of the nonpathogenic SAW 760 strain to human erythrocytes was enhanced by MAb to epitope 1 and blocked by galactose, confirming the presence of a functionally active lectin. A lectin radioimmunoassay based on MAb to epitopes 1 and 3 proved to be a simple and rapid method to distinguish pathogenic from nonpathogenic amebae in culture. Further exploration of the functional consequences of the antigenic differences demonstrated for the lectin may lead to a better understanding of its role in pathogenesis.
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PMID:Pathogenic and nonpathogenic strains of Entamoeba histolytica can be differentiated by monoclonal antibodies to the galactose-specific adherence lectin. 169 9

Entamoeba histolytica, a cause of invasive colitis or liver abscess, is responsible for substantial worldwide morbidity and mortality. An understanding of the biochemical basis for the parasite adherence and cytolytic activities and antiamebic host immune response mechanisms are prerequisites for vaccine development. The E. histolytica galactose (Gal) or N-acetyl-D-galactosamine (GalNAc) inhibitable adherence lectin mediates attachment of trophozoites to colonic mucins or mammalian target cells. Amebic cytolysis of target cells requires Gal/GalNAc-lectin-mediated adherence, parasite phospholipase A activity, and maintenance of an acid pH in amebic intracellular vesicles. Cytolytic activity is stimulated by phorbol esters (activators of protein kinase C) and results from an E. histolytica-mediated increase in free Ca++ within the target cell. The Gal/GalNAc adherence lectin is a highly conserved antigen that is universally recognized by human immune sera; patients cured of invasive amebiasis possess antigen-specific cell-mediated immunity effective in vitro against E. histolytica trophozoites. Promising vaccines include the purified adherence lectin, for eliciting an intestinal secretion of IgA antibody to lectin, and additional E. histolytica antigens, which elicit cell-mediated amebicidal responses.
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PMID:Entamoeba histolytica: from adherence to enteropathy. 253 86

Immunoprecipitation of Entamoeba histolytica proteins was performed with the sera of patients recovered from amebic liver abscess and colitis. The patients' amebic infection had been acquired in diverse areas of the world. The amebic galactose and N-acetyl-D-galactosamine-inhibitable adherence lectin was the major amebic antigen immunoprecipitated. The adherence lectin was recognized by all of the patients' sera tested regardless of the site (liver abscess vs. colitis) or geographic region that the amebic infection had occurred.
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PMID:Antigenic stability and immunodominance of the Gal/GalNAc adherence lectin of Entamoeba histolytica. 253 54

A spontaneously occurring experimental model of chronic colitis has been described in three closely related species of New World monkeys. One species, Saguinus oedipus oedipus, has the additional feature of developing adenocarcinoma of the colon in this setting. Pathological and lectin histochemistry studies were undertaken in 50 such colonic specimens to determine if pathological or histochemical features were associated with the concomitant development of cancer. Chronic inflammation was found in all of the colons examined, and 14% had features of acute inflammation, which was significantly associated with those animals that developed cancer. An oncofetal glycoconjugate structure has been defined in human colons by the ability to bind peanut lectin. A similar glycoconjugate, probably a mucin, was expressed in the colons of 65% of these animals. A marked degree of expression of the mucin was significantly associated with those animals that developed cancer. A highly significant association was found between the presence of acute inflammation and the expression of the mucin. These studies demonstrate similarities in glycoconjugate expression between the human colon and the New World monkey model of spontaneous colitis. A form of mucin is expressed in these animals that is highly associated with both the presence of acute inflammation and the development of cancer elsewhere in the colon. In addition, an association between acute inflammatory activity and neoplasia was found, suggesting a potential etiologic linkage between the two.
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PMID:Glycoconjugates in the colons of New World monkeys with spontaneous colitis. Association between inflammation and neoplasia. 310 6

Differences in colonic secretory glycoconjugates (ie, mucin) between normal and ulcerative colitis-prone patients have been noted. Similar differences may occur in a corresponding primate model, the cotton-top tamarin (CTT), Saguinus oedipus, a New World monkey which suffers from spontaneous chronic colitis and colon cancer. Lectin reagents were used to characterize and compare colonic cell surface, cytoplasmic, and secretory glycoconjugates of 9 clinically healthy cotton-top tamarins, 7 colitis-susceptible, cancer-resistant tamarins (Callithrix jacchus, Saguinus fuscicollis), and 8 colitis and cancer-resistant primates (Aotus trivirgatus, Saimiri sciureus, Macaca fascicularis, and Macaca mulatta). Paraffin-embedded colonic sections were labeled with ten different biotinylated lectins and visualized by the avidin-biotin peroxidase (ABC) method. Significant differences were demonstrated in the pattern of lectin staining between the colitis-resistant and colitis-prone groups of primates. The differences were noted with Griffonia simplicifolia-I (GS-I), Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA) before and after neuraminidase, Ricinus communis agglutinin-I (RCA-I), soybean agglutinin (SBA), Ulex europaeus agglutinin-I (UEA-I), wheat germ agglutinin (WGA), and succinylated WGA (S-WGA). Significant differences between the CTT and phylogenetically related colitis-prone but cancer-resistant tamarins were demonstrated with SBA, UEA-I, and PNA after desialylation with neuraminidase. These results suggest that differences in colonic cellular glycoconjugates between colitis- and cancer-susceptible species versus colitis-susceptible, cancer-resistant species may be associated with risk of cancer.
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PMID:Characterization of colonic cellular glycoconjugates in colitis and cancer-prone tamarins versus colitis and cancer-resistant primates. 313 57

In the preceding paper the authors demonstrated that the lectin staining patterns of normal colonic epithelium obtained from colitis and carcinoma-prone cotton top tamarins (CTTs), Saguinus oedipus, a New World primate, differs from colitis- and carcinoma-resistant primate species. In this study they determined the usefulness of cytochemical features in inflamed epithelium as indicators for malignant change. They compared the lectin staining pattern in inflamed mucosa and adjacent mucosa with colonic carcinoma from 8 CTTs with that of 9 clinically healthy CTTs with no histologic evidence of colitis. Deparaffinized sections were labeled with ten biotinylated lectins and stained by the avidin-biotin peroxidase complex method. Numerous significant differences were demonstrated in the lectin staining pattern between normal epithelium and colonic carcinoma; fewer between normal and chronic inflamed epithelium. However, between chronic inflamed epithelium and colonic carcinoma significant staining differences were observed with only two lectins, peanut agglutinin (PNA) and Ulex europaeus agglutinin-I (UEA-I). These findings suggest that there is a progression in alteration of lectin staining pattern from normal epithelium, via chronic colitis, to colonic carcinoma. Furthermore, the differences between chronic colitis and colonic carcinoma are expressed only with those lectins that are associated with malignant transformation of human colonic epithelium.
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PMID:Differences in cellular glycoconjugates of quiescent, inflamed, and neoplastic colonic epithelium in colitis and cancer-prone tamarins. 313 58

Humoral and mucosal IgA responses to a recombinant cysteine-rich portion (designated LC3) of the Entamoeba histolytica galactose-inhibitable lectin's 170-kDa subunit were determined in patients with amebic colitis. All patients had 170-kDa amebic antigen in serum, compared with 1 of 50 cyst passers and 1 of 31 controls (P < .01). Seven days after treatment, serum and fecal 170-kDa antigen became undetectable in 12 of the 13 patients (P < .001). Serum anti-LC3 IgA was found in 83.8% of colitis patients, compared with 2% of controls and 12% of asymptomatic cyst passers (P < .001). Salivary and fecal anti-LC3 IgA levels were higher in patients than in cyst passers (P < .001). In conclusion, in amebic colitis, development of humoral and mucosal IgA responses to the recombinant LC3-encoded protein correlates with detection of amebic 170-kDa antigen in serum and feces.
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PMID:Humoral and mucosal IgA antibody response to a recombinant 52-kDa cysteine-rich portion of the Entamoeba histolytica galactose-inhibitable lectin correlates with detection of native 170-kDa lectin antigen in serum of patients with amebic colitis. 865 85

Infection with the enteric parasite Entamoeba histolytica can result in colitis and dysentery as well as abscesses at extra-intestinal sites. An effective vaccine must be able to protect against both mucosal and systemic disease. In this study an attenuated Salmonella strain that expressed a portion of the GalNAc lectin of E, histolytica was used to orally immunize gerbils. Animals were challenged by intrahepatic injection of amebic trophozoites. A significant decrease in size of amebic liver abscesses was observed in orally immunized animals. Oral immunization with a Salmonella-based vaccine was as effective as systemic immunization for protection against systemic challenge.
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PMID:Protection in a gerbil model of amebiasis by oral immunization with Salmonella expressing the galactose/N-acetyl D-galactosamine inhibitable lectin of Entamoeba histolytica. 917 67

In the rabbit ileum Clostridium difficile toxin A causes inflammation and mucosal damage via a specific glycoprotein receptor that contains alpha-D-galactose. In rabbit colon toxin A also causes inflammation, and this is associated with increased myoelectric activity and eicosanoid production. The present in vitro study was undertaken to determine if a toxin A receptor on one or more layers of colonic smooth muscle could mediate the motor effects of this agent. Toxin A (20-100 microg/ml) was without effect on longitudinal and circular muscle but had two different effects on the muscularis mucosae. Initial exposure to the toxin caused increased numbers of spontaneous contractions and a small, atropine-, tetrodotoxin-, and indomethacin-resistant increase in resting tone. More importantly, however, 30-min exposure to toxin A resulted in attenuated muscularis mucosae responses to acetylcholine and K+. Both the small excitatory and the larger inhibitory effects of toxin A were abolished by pretreatment with the lectin BS-1, which binds to toxin A receptors, but not by the nonreceptor-binding lectin DBA. These data strongly suggest that toxin A causes significant motor effects on the distal colonic muscularis mucosae via a receptor-mediated mechanism. These mechanical data were supported by the presence of histologically demonstrable toxin A and BS-1 binding sites on the muscularis mucosae but not on either the longitudinal or circular muscle layers, both of which were unresponsive to the toxin. By depressing muscularis mucosae function and, ultimately, mucosal movement as a result of toxin A production, C. difficile may promote its own proliferation, thus further contributing to the development of antibiotic-associated colitis.
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PMID:In vitro evidence that rabbit distal colonic muscularis mucosae has a Clostridium difficile toxin A receptor. 972 50


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