Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed an enzymatic technique for isolating human intestinal mucosal lymphoid cells. This method was found to be superior to mechanical methods in regard to cell yield and survival. It is based on treating mucosa with serum-free solutions containing collagenase and deoxyribonuclease, followed by isolating the lymphoid cells through centrifugation steps involving fetal calf serum and ficoll-hypaque. Exposure of peripheral blood lymphocytes to the components of the enzymatic solution did not appreciably alter their uptake of tritiated thymidine in the presence or absence of mitogens. Application of the method to derive lymphoid cells from Crohn's disease, ulcerative colitis, and normal intestinal mucosa has shown that gut mucosal lymphocytes from inflammatory bowel disease (1) exceed the number of those from normal mucosa by a factor of 3 to 5; (2) show different degrees of tritiated thymidine uptake, spontaneously and in response to mitogens, depending upon the time they are harvested during the dissociation process; (3) are better stimulators than responders in the allogeneic mixed lymphocyte reaction; (4) generate suppressor cell activity comparable to that of peripheral blood lymphocytes; (5) cannot, in contrast to peripheral blood lymphocytes, generate antibody-dependent cell mediated cytotoxicity; and (6) produce an average of 5 times more IgM than equal numbers of peripheral blood lymphocytes.
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PMID:Gut mucosal lymphocytes in inflammatory bowel disease: isolation and preliminary functional characterization. 15 97

During cell proliferation, several "factors" are released into the microenvironment, or culture medium. The experiments described sought and examined agents that may cause or support malignant cell transformation. The response of colon cells from patients with ulcerative colitis (UC), familial polyposis coli (FPC) and colon carcinoma (CCC) to these agents was monitored by carcinoembryonic antigens (CEA) released into the medium during cell proliferation in a serum-free hormone-defined (SFHDM) medium, oncogenicity in athymic mice and colonigenicity, i.e. the ability of the cells to form colonies in soft agar. When cultured on the extracellular matrix (EM), i.e. footprints from colon carcinoma cells (short term or established cell lines), and in SFDHM, colon cells from patients with UC and FPC showed significant (P = 0.001) increases in all the three parameters. Analyses indicated that EM from cultures of [35S]methionine-labelled normal epithelial colon cells (NCE) differed from those left by UCC, FPC and CCC cell cultures. EM from NCE cell cultures did not contain [35S]methionine-labelled glycoproteins resistant to collagenase action which were not fragments of fibronectin, and which were present in EM from CCC cells. It is concluded that the extracellular matrix from malignant colon cells contains agents that support colon cell oncogenic transformation.
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PMID:Ulcerative colitis and familial polyposis oncologic transformation to colon carcinoma: changes in carcinoembryonic antigen release. 282 26

The clinical course of ulcerative colitis is characterized by recurring acute attacks and interspersed with periods of remission. The present study correlates the clinical, endoscopic and laboratory results in the follow-up of 22 rectocolitis patients in order to identify any data that might serve as a warning of recurrences. It is claimed that laboratory examinations like titering of alpha 1-antitrypsin, antithrombin III collagenase, C3 and C4 offer useful support for endoscopy which is generally considered the only reliable examination in the diagnosis of idiopathic rectocolitis.
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PMID:[Value of serology and endoscopy and clinical aspects in idiopathic rectocolitis]. 300 18

For a better understanding of local immunological factors in the pathogenesis of ulcerative colitis (UC), we isolated colonic mucosal lymphocytes (CML) from endoscopical biopsy specimens and studied their immunological characteristics. CML were isolated by a DTT-collagenase-cotton column method. Viability of isolated cells exceeded 90%, and the average yield per biopsy specimen was 1.2 +/- 0.6 X 10(4) (mean +/- SD). A large proportion of the CML isolated in this way were small lymphocytes and the numbers were higher in UC patients than in the controls. The percentage of T cells among the CML was higher in UC than in the controls, but the percentages of B cells did not differ. Peripheral blood lymphocytes from healthy controls showed very low levels of spontaneous synthesis of IgG, IgA, and IgM, but when cultured with PWM, these cells showed a high level of IgG and IgM synthesis but only a moderately elevated IgA production. In contrast, CML from healthy controls had a high level of spontaneous synthesis of IgG, IgA, and IgM; after culture with PWM, IgG synthesis roughly doubled and IgA synthesis increased tenfold compared with that of PBL. IgM synthesis was on the same level as in PBL. Although both PBL and CML cultured with PWM showed similar synthesis of IgG, IgA, and IgM in UC and healthy controls, the spontaneous synthesis of IgA and IgM in CML from patients with UC was approximately double that in the controls. Furthermore, in UC both PBL and CML had decreased Con A-induced suppressor-cell activity compared with controls. A defect of suppressor-cell activity and an increased number of T cells may play a role in the pathogenesis of UC.
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PMID:Cells isolated from endoscopical biopsy specimens. 316 Dec 60

A sensitive 4 h 51Cr-release cytotoxicity assay has been developed using as targets colonic epithelial cells obtained by Dispase-collagenase digestion of resected mucosa or colonoscopic biopsies. Peripheral blood mononuclear cells (MNC) from most healthy donors showed low, but significant levels of cytotoxicity for normal epithelial cell target cells of 8.7 (4.4) % (mean (SD] and similar levels were found in 14 ulcerative colitis (6.5 (4.4) %) and 16 Crohn's disease (6.2 (5.2) %) patients. Neither drug therapy nor disease activity influenced the results. The sensitivity of colonic epithelial cells isolated from inflamed and histologically normal mucosa to lysis by peripheral blood MNC from a single donor was not affected by the underlying disease. Anti-epithelial cell activity did not correlate with anti-K562 activity and the cytotoxic cell was plastic non-adherent and Leu-11b-. None of 15 MNC populations isolated from mucosa of normal, tumour bearing, or chronically inflamed intestine exhibited significant lysis of colonic epithelial cells despite killing of K562 target cells in 10. Lymphokine activated killer (LAK) cells, generated by interleukin-2 stimulation in vitro of nine intestinal and seven peripheral blood MNC populations, exhibited high levels of lysis of K562 cells but, on every occasion, failed to lyse colonic epithelial cells. These data indicate that spontaneously cytotoxic or LAK cells are unlikely to play a role in the generation of colonic epithelial cell injury by direct cytotoxicity in inflammatory bowel disease.
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PMID:Lysis of colonic epithelial cells by allogeneic mononuclear and lymphokine activated killer cells derived from peripheral blood and intestinal mucosa: evidence against a pathogenic role in inflammatory bowel disease. 326 5

The leakiness of the cell membranes of colonic epithelial cells isolated by the collagenase/Dispase technique from normal or diseased colons was assessed in a 4 h 51Cr release assay. Cells from normal, adenoma bearing or cancer bearing colons showed 51Cr release of 8% or less in almost all of 46 cell populations tested. In contrast, cells from mucosa affected by ulcerative colitis [11.9 (4.3%) n = 23] or Crohn's disease [8.4 (2.7%) n = 18] released significantly more 51Cr than the non-inflamed groups. Values are expressed as mean (SD). Overall, release values were greater in ulcerative colitis than Crohn's disease (p less than 0.01). In Crohn's disease, cells obtained from histologically inflamed mucosa released significantly more 51Cr [9.7 (2.5%) n = 11] than those from non-inflamed mucosa [6.4 (1.5%) n = 7, p less than 0.02] whereas, in ulcerative colitis, abnormal release values were found in 8 of 13 cell populations isolated from mucosa showing no histological evidence of active disease. In five patients with distal ulcerative colitis, cells from mucosa not apparently involved demonstrated normal 51Cr release in four of five studies despite abnormal release from cells from involved mucosa suggesting that a diffuse abnormality of the colonic epithelial cell is not usually present. These data indicate that chronic mucosal inflammation per se is associated with abnormalities of the colonic epithelial cell but that, in ulcerative colitis, the abnormality remains in many patients with quiescent disease. Identification of the local factors responsible for such an abnormality may contribute to an understanding of the pathogenesis of ulcerative colitis.
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PMID:Ulcerative colitis--a disease characterised by the abnormal colonic epithelial cell? 337 20

Lamina proprial lymphocytes (LPL), isolated by an EDTA-collagenase technique from patients with various colonic diseases, were investigated for LMIF release in vitro. On stimulation with the preparation of Kunin antigen, macrophage-depleted LPL from patients with severely or moderately active ulcerative colitis showed LMIF release which was significantly greater than that observed using LPL from patients with mild colitis or from those with other diseases of the large bowel, including Crohn's disease. Results similar to those obtained with LPL were found with the corresponding peripheral blood lymphocytes (PBL) stimulated by the preparation of Kunin antigen. In contrast, nonspecific stimulation in vitro with Concanavalin A showed no differences in LMIF releases by the LPL or PBL in the various disease groups. It is suggested that hypersensitivity to Kunin antigen may have pathogenic significance in ulcerative colitis.
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PMID:Leukocyte migration inhibitory factor (LMIF) release by human colonic lymphocytes. 627 Oct 90

Butyrate promotes epithelial cell healing and improves symptoms when administered rectally in patients with distal ulcerative colitis (UC). It was hypothesized that butyrate may enhance healing in patients with UC by stimulating colonocyte proliferation and/or protein production. Mucosa from the descending colon was obtained from patients with UC (n = 5), Crohn's disease (n = 8), diverticulitis (n = 6), and cancer (normal tissue 10 cm from tumor; n = 10). Epithelial cells were isolated using dispase/collagenase and differential sedimentation and incubated for 4 hr at 37 degrees C with either Na butyrate (10 mM) or NaCl (10 mM). Protein synthesis was assessed by [14C]leucine incorporation and proliferation was determined with [3H]thymidine. Mean viability and purity were >88%. Spontaneous proliferation was significantly increased in UC when compared to diverticulitis and normal controls. Butyrate significantly increased protein synthesis in UC epithelial cells when compared to saline control. The therapeutic effects of butyrate in patients with UC may be due to its use by epithelial cells as a metabolic fuel to increase protein production and promote healing.
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PMID:Butyrate increases colonocyte protein synthesis in ulcerative colitis. 804 Nov 40

Very little is currently known regarding the underlying mechanisms involved in the etiology of intestinal strictures in chronic inflammatory bowel disease. The deposition of extracellular matrix components, especially collagens, is thought to play an important role in the etiology of intestinal strictures. The main goal of this study was therefore to investigate the collagen metabolism in patients with inflammatory bowel disease using the in situ hybridization technique. We determined de novo synthesis of the (pro)-collagen mRNA transcripts alpha 1I, alpha 1III, alpha 1IV, alpha 2V as well as the collagen degrading enzyme mRNA transcripts collagenase type I and IV in Crohn's disease and ulcerative colitis and compared the rate of expression semiquantitatively to healthy controls. We found a significant increase of all (pro)-collagen transcripts tested in Crohn's disease and ulcerative colitis as compared to healthy control tissues, indicating an increased de novo synthesis of all collagens in both inflammatory bowel diseases. However, we observed a significant difference in the expression of the collagenase mRNA transcripts between Crohn's disease and ulcerative colitis. Compared to healthy control subjects we were unable to detect a significant difference in the expression of collagenase type I and IV in Crohn's disease; in contrast, we observed a significant increase in the rate of expression for the collagenases in ulcerative colitis as compared to controls or biopsies from patients with Crohn's disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Indications for different collagen metabolism in Crohn disease and ulcerative colitis]. 849 73

The expression of MMP-7 (pump-1) gene was examined in 10 cases of colorectal cancer by utilizing RT-PCR. In 9 out of 10 cases, MMP-7 mRNA was detected in cancerous tissue, whereas none was detected in adjacent normal colon tissue. However, this message was detected in only 1 out of 6 colon-cancer cell lines. In colonic mucosa from 3 patients with ulcerative colitis it was not detected. The expression of MMP-2 (72-kDa type-IV collagenase) mRNA was also investigated in the same tissue samples, and was detected in all samples, including cancerous and non-cancerous tissue. Our data suggest that MMP-7 is expressed in a tumor-associated manner in colorectal cancers and may play a role in tumor progression.
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PMID:Expression of MMP-7(PUMP-1) mRNA in human colorectal cancers. 851 52


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