The clinical course of ulcerative colitis (UC) is unpredictable. The need for reliable biomarkers to reflect disease severity and predict disease course is therefore large. We investigated whether cytokines in mucosal tissue and serum reflect clinical disease severity at the onset of UC and predict the future disease course.
We prospectively monitored 102 patients from the onset of UC during 3 years, and they were followed up yearly for clinical and biochemical disease severity. Rectal biopsies were obtained from healthy controls and patients with UC. Serum and stool samples were obtained from patients with UC. Total mRNA from biopsies was analyzed with real-time PCR. Cytokine levels in serum were determined using Luminex or ELISA.
Mucosal mRNA expression of IL-17A was 99.8 times higher while IFN-γ and IL-13 expression was increased 12.4 and 6.7 times, respectively, in patients relative to controls. Serum IL-17A correlated with clinical disease severity at the onset. Also, contrary to a number of other parameters, serum IL-17A at the onset predicted the clinical and biochemical course of the disease, as reflected by the Mayo score, number × severity of flares, and fecal calprotectin levels, respectively, during 3 years after the onset of the disease. None of these associations were found with mucosal cytokines at the onset.
Serum IL-17A levels of treatment-naive patients with UC reflect clinical disease severity at the onset of the disease and also predicted the disease course over the following 3 years. Thus, serum IL-17A may be valuable in the clinical management of patients with UC at the onset of the disease.
Article first published online 20 August 2013
Departments of *Internal Medicine and Clinical Nutrition and
†Microbiology and Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;
‡Translational Research Center for Gastrointestinal Disorders (TARGID), Department of Clinical and Experimental Medicine, University of Leuven, Leuven, Belgium.
Reprints: Lena Öhman, PhD, Department of Microbiology and Immunology, University of Gothenburg, Medicinaregatan 7A, Gothenburg 413 46, Sweden (e-mail: email@example.com).
Supported by The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Swedish Medical Research Council (grants 13409, 21691, and 21692 to M.S. and 22273 to L.Ö.), The Marianne and Marcus Wallenberg Foundation, and The Swedish Society of Medicine.
The authors have no conflicts of interest to disclose.
Received June 11, 2013
Accepted July 16, 2013