Original ResearchBasic and Translational—Alimentary TractDefective Leukocyte GM-CSF Receptor (CD116) Expression and Function in Inflammatory Bowel Disease
Section snippets
Human Subjects
The institutional review board of the University of Colorado Denver approved all human studies. CD and UC patients were diagnosed using established criteria and CD phenotype per the Montreal criteria12 (see Table 1 for patient characteristics). Irritable bowel syndrome (IBS) patients were diagnosed by ROME III criteria.13 Rheumatoid arthritis patients were diagnosed based on criteria of the American College of Rheumatology.14 Medications were recorded at time of blood draws and the attending
Results
Initial studies were undertaken to define the levels of CD116 messenger RNA in IBD and control granulocytes. As shown in Figure 1A, real-time PCR analyses for CD116 were compared in 10 healthy controls and 10 patients with IBD. As can be seen, CD116 messenger RNA levels were decreased by as much as 65% ± 8% in IBD granulocytes (P < .001). Defective CD116 expression was evident in both UC and CD, but not in granulocytes from patients with IBS (Figure 1A). To examine the specificity of this
Discussion
Given the unknown etiology of IBD, there is significant interest in both new therapies and biomarkers to define and subdivide patient populations. GM-CSF has attracted attention of late as a therapy for disorders of innate immunity, including IBD.5 In this study, we sought to define whether specific differences existed in CD116 expression between IBD and healthy control patients. Results from the present studies show that decreased expression and function of CD116 is a distinguishing feature of
Acknowledgments
Drs Goldstein and Kominsky contributed equally to this work.
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Conflicts of interest The authors disclose no conflicts.
Funding This work was supported by National Institutes of Health grants R37-DK5018, RO1-HL60569, and by support from the Crohn's and Colitis Foundation of America.