caa a22 4500 475748549 CHVBK 20180406123520.0 cr unu---uuuuu 170329e20000901xx s 000 0 eng 10.1023/A:1006672114184 doi (NATIONALLICENCE)springer-10.1023/A:1006672114184 IL-10 Secretion and Sensitivity in Normal Human Intestine and Inflammatory Bowel Disease [Elektronische Daten] [Christoph Gasche, Silvia Bakos, Clemens Dejaco, Wolfgang Tillinger, Schaker Zakeri, Walter Reinisch] Interleukin-10 (IL-10) deficiency in gene knockout mice causes chronic enterocolitis. We hypothesized that inflammation in human inflammatory bowel disease might result from innate alterations in the IL-10 pathway. Serum, supernatants, and mRNA of peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) derived from inflamed (LPMC-i) and noninflamed colonic mucosa (LPMC-ni) were collected from patients with Crohn's colitis, ulcerative colitis, and controls. IL-10 protein concentrations and IL-10 mRNA were examined in response to PMA/CD3 or PHA stimulation. The response to rhIL-10 was assessed by inhibition of tumor necrosis factor-alpha (TNF-α), IL-6, and interferon-gamma (IFN-γ) production. Serum IL-10 levels of inflammatory bowel disease (IBD) patients were within the normal range. IL-10 concentrations in supernatants from LPMC-i were significantly lower than from LPMC-ni or PBMC. No difference was seen between samples from ulcerative colitis and Crohn's disease. IL-10 mRNA was detected in 0/4 LPMC-i samples compared to 1/6 LPMC-ni and 6/6 PBMC. RhIL-10 inhibited TNF-α, IL-6, and IFN-γ synthesis in PBMC. This effect was strongly diminished in LPMC. Disease-specific alterations were not detected. Our data suggest that LPMC derived from inflamed colonic mucosa have a reduced ability to produce and to respond to rhIL-10. A disease-specific alteration in the IL-10 pathway, however, was not found. Plenum Publishing Corporation, 2000 Inflammatory bowel disease nationallicence interleukin-10 nationallicence Lamina propria mononuclear cells nationallicence Gasche Christoph Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Bakos Silvia Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Dejaco Clemens Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Tillinger Wolfgang Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Zakeri Schaker Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Reinisch Walter Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut Journal of Clinical Immunology Kluwer Academic Publishers-Plenum Publishers 20/5(2000-09-01), 362-370 0271-9142 20:5<362 2000 20 10875 https://doi.org/10.1023/A:1006672114184 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1006672114184 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Gasche Christoph Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 700 1- Bakos Silvia Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 700 1- Dejaco Clemens Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 700 1- Tillinger Wolfgang Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 700 1- Zakeri Schaker Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 700 1- Reinisch Walter Department of Gastroenterology and Hepatology, University of Vienna, Vienna, Austria aut NATIONALLICENCE 773 0- Journal of Clinical Immunology Kluwer Academic Publishers-Plenum Publishers 20/5(2000-09-01), 362-370 0271-9142 20:5<362 2000 20 10875 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer