AIM： To investigate intestinal alkaline phosphatase （iAP） in the intestinal mucosa of children with inflammatory bowel disease （IBD）. METHODS： Colonic biopsy samples were taken from 15 newly diagnosed IBD patien...AIM： To investigate intestinal alkaline phosphatase （iAP） in the intestinal mucosa of children with inflammatory bowel disease （IBD）. METHODS： Colonic biopsy samples were taken from 15 newly diagnosed IBD patients and from 10 healthy controls. In IBD patients, specimens were obtainedboth from inflamed and non-inflamed areas. The lAP mRNA and protein expression was determined by reverse transcription-polymerase chain reaction and Western blotting analysis, respectively. Tissue localiza- tion of lAP and Toll-like receptor （TLR） 4 was investi- gated by immunofluorescent staining. RESULTS： The lAP protein level in the inflamed muco- sa of children with Crohn＇s disease （CD） and ulcerative colitis （UC） was significantly decreased when compared with controls （both P 〈 0.05）. Similarly, we found a significantly decreased level of lAP protein in the in- flamed mucosa in CD compared with non-inflamed mucosa in CD （P 〈 0.05）. In addition, the iAP protein level in inflamed colonic mucosa in patients with UC was decreased compared with non-inflamed mucosa in patients with CD （P 〈 0.05）. lAP protein levels in the non-inflamed mucosa of patients with CD were similar to controls, lAP mRNA expression in inflamed colonic mucosa of children with CD and UC was not significant- ly different from that in non-inflamed colonic mucosa with CD. Expression of lAP mRNA in patients with non- inflamed mucosa and in controls were similar. Co-local- ization of lAP with TLR4 showed intense staining with a dotted-like pattern, lAP was present in the inflamed and non-inflamed mucosa of patients with CD, UC, and in control biopsy specimens, irrespective of whether it was present in the terminal ileum or in the colon. However, the fluorescent signal of TLR4 was more pro- nounced in the colon compared with the terminal ileum in all groups studied. CONCLUSION： Lower than normal lAP protein levels in inflamed mucosa of IBD patients may indicate a role for lAP in inflammatory lesions in IBD. Based on our results, administration of exogenous lAP enzyme to pa- tients with the active form of IBD may be a therapeutic option.展开更多
AIM： A few studies have applied genomic-wide gene expression analysis in inflamed colon tissue sample in ulcerative colitis （UC）. We reported the first study of non-inflamed mucosal gene expression in UC and explor...AIM： A few studies have applied genomic-wide gene expression analysis in inflamed colon tissue sample in ulcerative colitis （UC）. We reported the first study of non-inflamed mucosal gene expression in UC and explored its clinical implication. METHODS： Non-inflamed mucosa was obtained from 6 UC patients who received total colectomy. The gene expression of UC in noninflamed mucosa was monitored with a microarray. For a selected gene, RT-PCR was performed to verify array results and to further examine expression pattern in inflamed mucosa of UC, colorectal cancer tissue and normal mucosa using additional matched pairs. RESULTS： Two genes showing 2.5-fold decreased expression with significance set at in UC samples were borneo box a4 （HOXa4） and mads box transcription enhancer factor 2, polypeptide B （MEF2b）. RT-PCR showed that MEF2b expression in non-inflamed mucosa was significantly downregulated, whereas the expression of MEF2b increased in accordance with the severity of mucosal inflammation. HOXa4 expression both in inflamed and non-inflamed mucosa in UC was consistently downregulated, and the downregulation of HOXa4 was also found in colorectal carcinoma. CONCLUSION： It is suggested that the MEF2b expression in UC which increase in accordance with inflammation may be induced by the inflammatory mediator. In contrast the downregulation of HOXa4 may be partly involved in the pathogenesis of disease including UC and UC-related carcinogenesis.展开更多
AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer.METHODS: A total of 99 patients with ...AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer.METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori(H pylori) study. Out of these cases,44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of Hpylori in the stomach was then studied.RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without Hpyloricolonization in the stomach (P＜0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03).CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer.A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.展开更多
To propose a new pathogenesis called Radical Induction to explain the genesis and progression of ulcerative colitis (UC). UC is an inflammatory bowel disease. Colonic inflammation in UC is mediated by a buildup of whi...To propose a new pathogenesis called Radical Induction to explain the genesis and progression of ulcerative colitis (UC). UC is an inflammatory bowel disease. Colonic inflammation in UC is mediated by a buildup of white blood cells (WBCs) within the colonic mucosal lining; however,to date there is no answer for why WBCs initially enter the colonic mucosa to begin with. A new pathogenesis termed 'Radical Induction Theory' is proposed to explain this and states that excess un-neutralized hydrogen peroxide, produced within colonic epithelial cells as a result of aberrant cellular metabolism, diffuses through cell membranes to the extracellular space where it is converted to the highly damaging hydroxyl radical resulting in oxidative damage to structures comprising the colonic epithelial barrier. Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens from invading the normally sterile submucosa. This antigenic exposure provokes an initial immune response of WBC infiltration into the colonic mucosa. Once present in the mucosa,WBCs are stimulated to secrete toxins by direct exposure to fecal bacteria leading to mucosal ulceration and bloody diarrhea characteristic of this disease.展开更多
AIM:To assess B1a cell expression in the rectal mucosa of ulcerative colitis (UC) patients in comparison with healthy controls.METHODS:Rectal mucosa biopsies were collected from 15 UC patients and 17 healthy controls....AIM:To assess B1a cell expression in the rectal mucosa of ulcerative colitis (UC) patients in comparison with healthy controls.METHODS:Rectal mucosa biopsies were collected from 15 UC patients and 17 healthy controls.CD5 + B cells were analysed by three colour flow cytometry from rectal mucosal samples after mechanical disaggregation by Medimachine.Immunohistochemical analysis of B and T lymphocytes was also performed.Correlations between,on the one hand,rectal B1a cell concentrations and,on the other,erythrocyte sedimentation rate and C-reactive protein levels and clinical,endoscopic and histological disease activity indices were evaluated.RESULTS:Rectal B-lymphocyte (CD19 + /CD45 +) rate and concentration were higher in UC patients compared with those in healthy controls (47.85% ± 3.12% vs 26.10% ± 3.40%,P=0.001 and 501 ± 91 cells/mm 2 vs 117 ± 18 cells/mm 2,P < 0.001);Rectal B1a cell density (CD5 + CD19 +) was higher in UC patients than in healthy controls (85 ± 15 cells/mm 2 vs 31 ± 6.7 cells/mm 2,P=0.009).Rectal B1a cell (CD5/CD19 +) rate correlated inversely with endoscopic classification (Rs=-0.637,P < 0.05).CONCLUSION:B1a lymphocytes seem to be involved in the pathogenesis of UC,however,the role they play in its early phases and in disease activity,have yet to be defined.展开更多
基金Supported by Grants OTKA-76316,OTKA-K81117,and ETT-028-02 (Veres G and Vannay á are holders of the János Bolyai Research grant)János Bolyai Research Scholarship of the Hungarian Academy of Sciences
文摘AIM： To investigate intestinal alkaline phosphatase （iAP） in the intestinal mucosa of children with inflammatory bowel disease （IBD）. METHODS： Colonic biopsy samples were taken from 15 newly diagnosed IBD patients and from 10 healthy controls. In IBD patients, specimens were obtainedboth from inflamed and non-inflamed areas. The lAP mRNA and protein expression was determined by reverse transcription-polymerase chain reaction and Western blotting analysis, respectively. Tissue localiza- tion of lAP and Toll-like receptor （TLR） 4 was investi- gated by immunofluorescent staining. RESULTS： The lAP protein level in the inflamed muco- sa of children with Crohn＇s disease （CD） and ulcerative colitis （UC） was significantly decreased when compared with controls （both P 〈 0.05）. Similarly, we found a significantly decreased level of lAP protein in the in- flamed mucosa in CD compared with non-inflamed mucosa in CD （P 〈 0.05）. In addition, the iAP protein level in inflamed colonic mucosa in patients with UC was decreased compared with non-inflamed mucosa in patients with CD （P 〈 0.05）. lAP protein levels in the non-inflamed mucosa of patients with CD were similar to controls, lAP mRNA expression in inflamed colonic mucosa of children with CD and UC was not significant- ly different from that in non-inflamed colonic mucosa with CD. Expression of lAP mRNA in patients with non- inflamed mucosa and in controls were similar. Co-local- ization of lAP with TLR4 showed intense staining with a dotted-like pattern, lAP was present in the inflamed and non-inflamed mucosa of patients with CD, UC, and in control biopsy specimens, irrespective of whether it was present in the terminal ileum or in the colon. However, the fluorescent signal of TLR4 was more pro- nounced in the colon compared with the terminal ileum in all groups studied. CONCLUSION： Lower than normal lAP protein levels in inflamed mucosa of IBD patients may indicate a role for lAP in inflammatory lesions in IBD. Based on our results, administration of exogenous lAP enzyme to pa- tients with the active form of IBD may be a therapeutic option.
文摘AIM： A few studies have applied genomic-wide gene expression analysis in inflamed colon tissue sample in ulcerative colitis （UC）. We reported the first study of non-inflamed mucosal gene expression in UC and explored its clinical implication. METHODS： Non-inflamed mucosa was obtained from 6 UC patients who received total colectomy. The gene expression of UC in noninflamed mucosa was monitored with a microarray. For a selected gene, RT-PCR was performed to verify array results and to further examine expression pattern in inflamed mucosa of UC, colorectal cancer tissue and normal mucosa using additional matched pairs. RESULTS： Two genes showing 2.5-fold decreased expression with significance set at in UC samples were borneo box a4 （HOXa4） and mads box transcription enhancer factor 2, polypeptide B （MEF2b）. RT-PCR showed that MEF2b expression in non-inflamed mucosa was significantly downregulated, whereas the expression of MEF2b increased in accordance with the severity of mucosal inflammation. HOXa4 expression both in inflamed and non-inflamed mucosa in UC was consistently downregulated, and the downregulation of HOXa4 was also found in colorectal carcinoma. CONCLUSION： It is suggested that the MEF2b expression in UC which increase in accordance with inflammation may be induced by the inflammatory mediator. In contrast the downregulation of HOXa4 may be partly involved in the pathogenesis of disease including UC and UC-related carcinogenesis.
文摘AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer.METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori(H pylori) study. Out of these cases,44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of Hpylori in the stomach was then studied.RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without Hpyloricolonization in the stomach (P＜0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03).CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer.A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.
文摘To propose a new pathogenesis called Radical Induction to explain the genesis and progression of ulcerative colitis (UC). UC is an inflammatory bowel disease. Colonic inflammation in UC is mediated by a buildup of white blood cells (WBCs) within the colonic mucosal lining; however,to date there is no answer for why WBCs initially enter the colonic mucosa to begin with. A new pathogenesis termed 'Radical Induction Theory' is proposed to explain this and states that excess un-neutralized hydrogen peroxide, produced within colonic epithelial cells as a result of aberrant cellular metabolism, diffuses through cell membranes to the extracellular space where it is converted to the highly damaging hydroxyl radical resulting in oxidative damage to structures comprising the colonic epithelial barrier. Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens from invading the normally sterile submucosa. This antigenic exposure provokes an initial immune response of WBC infiltration into the colonic mucosa. Once present in the mucosa,WBCs are stimulated to secrete toxins by direct exposure to fecal bacteria leading to mucosal ulceration and bloody diarrhea characteristic of this disease.
文摘AIM:To assess B1a cell expression in the rectal mucosa of ulcerative colitis (UC) patients in comparison with healthy controls.METHODS:Rectal mucosa biopsies were collected from 15 UC patients and 17 healthy controls.CD5 + B cells were analysed by three colour flow cytometry from rectal mucosal samples after mechanical disaggregation by Medimachine.Immunohistochemical analysis of B and T lymphocytes was also performed.Correlations between,on the one hand,rectal B1a cell concentrations and,on the other,erythrocyte sedimentation rate and C-reactive protein levels and clinical,endoscopic and histological disease activity indices were evaluated.RESULTS:Rectal B-lymphocyte (CD19 + /CD45 +) rate and concentration were higher in UC patients compared with those in healthy controls (47.85% ± 3.12% vs 26.10% ± 3.40%,P=0.001 and 501 ± 91 cells/mm 2 vs 117 ± 18 cells/mm 2,P < 0.001);Rectal B1a cell density (CD5 + CD19 +) was higher in UC patients than in healthy controls (85 ± 15 cells/mm 2 vs 31 ± 6.7 cells/mm 2,P=0.009).Rectal B1a cell (CD5/CD19 +) rate correlated inversely with endoscopic classification (Rs=-0.637,P < 0.05).CONCLUSION:B1a lymphocytes seem to be involved in the pathogenesis of UC,however,the role they play in its early phases and in disease activity,have yet to be defined.
