Ondrej Fabian1,2,3, Adam Klocperk4, Tereza Lerchova5, Pavla Jencova6, Lucie Stolova6, Marie Belhajova6, Dagmar Voriskova6, Denis Kazeka5, Ales Vicha6, Ondrej Hradsky5, Jiri Bronsky5. 1. Clinical and Transplant Pathology Centre, Institute for Clinical and Experimental Medicine, Videnska 1958/9, Prague 4, 140 21, Czech Republic. ondrej.fabian@ikem.cz. 2. Department of Pathology and Molecular Medicine, 3Rd Faculty of Medicine, Charles University and Thomayer Hospital, Videnska 800, Prague 4, 140 59, Czech Republic. ondrej.fabian@ikem.cz. 3. Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84, Prague 5, 150 06, Czech Republic. ondrej.fabian@ikem.cz. 4. Department of Immunology, 2Nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84, Prague 5, 150 06, Czech Republic. 5. Gastroenterology and Nutrition Unit, Department of Paediatrics, 2Nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84, Prague 5, 150 06, Czech Republic. 6. Department of Paediatric Haematology and Oncology, 2Nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84, Prague 5, 150 06, Czech Republic.
Abstract
BACKGROUND: Inflammatory bowel diseases (IBD) frequently manifest in pediatric age, but may have atypical clinical, histological and laboratory features. Their underlying immune pathophysiology is incompletely understood, rendering quick diagnosis followed by tailored therapy difficult. The tumor necrosis factor superfamily receptor CD30 has been proposed as a potential marker of ulcerative colitis (UC) and has also been associated with elevated Th2 helper T cells. METHODS: A cohort of pediatric patients with UC and Crohn's disease (CD) was evaluated for serum soluble CD30 (sCD30) using ELISA and expression of CD30 and subpopulations of Th1/Th2/Th17 lymphocytes in the gastrointestinal mucosa using flow cytometry (FCM). The dataset is supported by endoscopic and microscopic activity of the disease and basic laboratory markers of inflammation. RESULTS: The cohort consisted of 102 observations from 94 patients. sCD30 levels did not differ between patients with CD or UC. However, sCD30 levels correlated with levels of CRP, ESR, fecal calprotectin and albumin and also with clinical activity of the disease in patients with both UC and CD. FCM was not helpful in evaluation of mucosal CD30, which was lowly expressed and not associated with the diagnosis or disease activity. We show augmented Th2 and Th1/17 response in terminal ileum and right-sided colon and decreased Th1/17 response in left-sided colon of UC patients. T lymphocyte subsets were also affected by anti-TNF treatment and patients' age. CONCLUSIONS: Neither sCD30 nor mucosal CD30 expression was helpful in differentiating between UC and CD. sCD30 seems to reflect a degree of systemic inflammation and clinical activity in IBD.
BACKGROUND: Inflammatory bowel diseases (IBD) frequently manifest in pediatric age, but may have atypical clinical, histological and laboratory features. Their underlying immune pathophysiology is incompletely understood, rendering quick diagnosis followed by tailored therapy difficult. The tumor necrosis factor superfamily receptor CD30 has been proposed as a potential marker of ulcerative colitis (UC) and has also been associated with elevated Th2 helper T cells. METHODS: A cohort of pediatric patients with UC and Crohn's disease (CD) was evaluated for serum soluble CD30 (sCD30) using ELISA and expression of CD30 and subpopulations of Th1/Th2/Th17 lymphocytes in the gastrointestinal mucosa using flow cytometry (FCM). The dataset is supported by endoscopic and microscopic activity of the disease and basic laboratory markers of inflammation. RESULTS: The cohort consisted of 102 observations from 94 patients. sCD30 levels did not differ between patients with CD or UC. However, sCD30 levels correlated with levels of CRP, ESR, fecal calprotectin and albumin and also with clinical activity of the disease in patients with both UC and CD. FCM was not helpful in evaluation of mucosal CD30, which was lowly expressed and not associated with the diagnosis or disease activity. We show augmented Th2 and Th1/17 response in terminal ileum and right-sided colon and decreased Th1/17 response in left-sided colon of UC patients. T lymphocyte subsets were also affected by anti-TNF treatment and patients' age. CONCLUSIONS: Neither sCD30 nor mucosal CD30 expression was helpful in differentiating between UC and CD. sCD30 seems to reflect a degree of systemic inflammation and clinical activity in IBD.