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| 1 | Gut barrier failure biomarkers are associated with poor disease outcome in patients with primary sclerosing cholangitis显示文摘AIM To assess the prevalence of a panel of serologic markers that reflect gut barrier dysfunction in a mixed cohort of pediatric and adult primary sclerosing cholangitis(PSC) patients.METHODS Sera of 67 PSC patients [median age(range): 32(5-79) years, concomitant IBD: 67% and cirrhosis: 20%] were assayed for the presence of antibodies against to F-actin(AAA Ig A/Ig G) and gliadin(AGA Ig A/Ig G)] and for serum level of intestinal fatty acid-binding protein(I-FABP) by ELISA. Markers of lipopolysaccharide(LPS) exposure [LPS binding protein(LBP)] and various antimicrobial antibodies [anti-OMP Plus Ig A and endotoxin core Ig A antibody(Endo CAb)] were also determined. Poor disease outcome was defined as orthotopic liver transplantation and/or liver-related death during the follow-up [median: 99(14-106) mo]. One hundred and fifty-three healthy subjects(HCONT) and 172 ulcerative colitis(UC) patients were the controls. RESULTS A total of 28.4%, 28.0%, 9% and 20.9% of PSC patients were positive for AAA Ig A, AAA Ig G, AGA Ig A and AGA Ig G, respectively. Frequencies of AAA Ig A and AAA Ig G(P < 0.001, for both) and AGA Ig G(P = 0.01, for both) but not AGA Ig A were significantly higher compared to both of the HCONT and the UC groups. In survival analysis, AAA Ig A-positivity was revealed as an independent predictor of poor disease outcome after adjusting either for the presence of cirrhosis [HR = 5.15(1.27-20.86), P = 0.022 or for the Mayo risk score(HR = 4.24(0.99-18.21), P = 0.052]. AAA Ig A-positivity was significantly associated with higher frequency of antimicrobial antibodies(P < 0.001 for Endo Cab Ig A and P = 0.012 for anti-OMP Plus Ig A) and higher level of the enterocyte damage marker(median I-FABP_(AAA Ig A pos vs neg): 365 vs 166 pg/m L, P = 0.011), but not with serum LBP level. CONCLUSION Presence of Ig A type AAA identified PSC patients with progressive disease. Moreover, it is associated with enhanced mucosal immune response to various microbial antigens and enterocyte damage further highlighting the importance of the gut-liver interaction in PSC. | Tamas Tornai Eszter Palyu Zsuzsanna Vitalis Istvan Tornai David Tornai Peter Antal-Szalmas Gary L Norman Zakera Shums Gabor Veres Antal Dezsofi Gabriella Par Alajos Par Peter Orosz Ferenc Szalay Peter Laszlo Lakatos Maria Papp | 2017 | World Journal of Gastroenterology2017，23，29： | 5 |
| 2 | Increased expression of Toll-like receptor (TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease 显示文摘 | SZEBENI B VERES G DEZSOFI A | 2008 | Clin Exp Immunol2008，151，1： | 1 |
| 3 | Increased expression of Toll-like receptor (TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease 显示文摘 | Szebeni B Veres G Dezsofi A | 2007 | Clin Exp lmmunol2007，151，： | 1 |
| 4 | Increased expression of Toll-like receptor TLR2 and TLR4 in the colonic mucosa显示文摘 | Szebeni B Veres G Dezsofi A eta/ | 2007 | Clin Exp interleukin-17 aggravates dextran sulfate immunol2007，151，1： | 1 |
| 5 | Increased expression of Toll-like receptor(TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease显示文摘 | SZEBENI B VERES G DEZSOFI A | 2008 | Clin Exp Immunol2008，151，： | 1 |
| 6 | Increased expression of Toll- like receptor(TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease显示文摘 | Szebeni B Veres G Dezsofi A | 2008 | Clin Exp Immunol2008，151，1： | 1 |
| 7 | Pancreatic Autoantibodies and Autoantibodies Against Goblet Cells in Pediatric Patients With Inflammatory Bowel Disease显示文摘 | Marta Kovacs Peter Laszlo Lakatos Maria Papp Silvia Jacobsen Eva Nemes Marianne Polgar Eniko Solyom Piroska Bodi Agnes Horvath Katalin Eszter Muller Kriszta Molnar Doloresz Szabo Aron Cseh Antal Dezsofi Andras Arato Gabor Veres | 2012 | Journal of Pediatric Gastroenterology and Nutrition2012，，4： | 1 |
| 8 | Increased expression of Toll -like receptor (TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease 显示文摘 | SZEBENI B VERES G DEZSOFI A | 2008 | Clin Exp Immunol2008，151，1： | 1 |
| 9 | Immune phenotype in children with therapy-nave remitted and relapsed Crohn’s disease显示文摘AIM: To characterize the prevalence of subpopulations of CD4+ cells along with that of major inhibitor or stimulator cell types in therapy-nave childhood Crohn's disease (CD) and to test whether abnormalities of immune phenotype are normalized with the improvement of clinical signs and symptoms of disease. METHODS: We enrolled 26 pediatric patients with CD. 14 therapy-nave CD children; of those, 10 children remitted on conventional therapy and formed the remission group. We also tested another group of 12 chil-dren who relapsed with conventional therapy and were given infliximab; and 15 healthy children who served as controls. The prevalence of Th1 and Th2, nave and memory, activated and regulatory T cells, along with the members of innate immunity such as natural killer (NK), NK-T, myeloid and plasmocytoid dendritic cells (DCs), monocytes and Toll-like receptor (TLR)-2 and TLR-4 expression were determined in peripheral blood samples. RESULTS: Children with therapy-nave CD and those in relapse showed a decrease in Th1 cell prevalence. Simultaneously, an increased prevalence of memory and activated lymphocytes along with that of DCs and monocytes was observed. In addition, the ratio of myeloid /plasmocytoid DCs and the prevalence of TLR-2 or TLR-4 positive DCs and monocytes were also higher in therapy-nave CD than in controls. The majority of alterations diminished in remitted CD irrespective of whether remission was obtained by conventional or biological therapy. CONCLUSION: The finding that immune phenotype is normalized in remission suggests a link between immune phenotype and disease activity in childhood CD. Our observations support the involvement of members of the adaptive and innate immune systems in childhood CD. | Aron Cseh Barna Vasarhelyi Kriszta Molnar Balazs Szalay Peter Svec Andras Treszl Antal Dezsofi Peter Laszlo Lakatos Andras Arato Tivadar Tulassay Gabor Veres | 2010 | World Journal of Gastroenterology2010，16，47： | 0 |
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