Chemokine and cytokine levels in inflammatory bowel disease patients |
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| Institution: | 1. Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA;2. Department of Cell and Developmental Biology, University of South Carolina, Columbia, SC 29208, USA;3. Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA;1. Department of Gastroenterology, Sheba Medical Center Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel;3. Institute of Clinical Pharmacology, Sheba Medical Center Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel;4. Israel Rambam Health Care Campus and Bruce Rappaport School of Medicine, Technion Institute of Technology, Haifa, Israel;1. Department of Immunology, Dalian Medical University, Dalian, Liaoning, China;2. Department of Microecology, Dalian Medical University, Dalian, Liaoning, China;3. Institute of Biotechnology, Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan;4. The Division of Respirology, Critical Care and Sleep Medicine, Royal University Hospital, University of Saskatchewan, Saskatoon, Canada;1. F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Medical Genetics Research Institute, Cedars-Sinai Medical Center, Los Angeles, California;2. Department of Pediatrics and Human Genetics, Emory University School of Medicine, and Children’s Healthcare of Atlanta, Atlanta, Georgia;3. Departments of Genetics and Medicine, Division of Gastroenterology, Icahn School of Medicine at Mount Sinai, New York, New York;1. Department of Pharmacology and Cancer Biology, Duke University, Durham, NC 27710, USA;2. Departments of Biochemistry and Radiation Oncology, University of Texas, Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA;3. Department of Chemistry, Duke University, Durham, NC 27710, USA;4. University of Michigan, Division of Rheumatology and Clinical Autoimmunity Center of Excellence, Ann Arbor, MI 48109, USA;5. Department of Applied Biology, Jordan University of Science and Technology, PO Box 3030, Irbid 22110, Jordan;1. Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Cincinnati College of Medicine and the Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio;2. Department of Human Genetics, Emory University, Atlanta, Georgia;3. Department of Pediatrics, Emory University, Atlanta, Georgia;4. Cancer and Blood Disease Institute, Department of Pediatrics, University of Cincinnati College of Medicine and the Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio;5. Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio;6. Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Canada;7. Department of Pediatrics, University of Pennsylvania, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania;8. Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Medical College of Wisconsin, Milwaukee, Wisconsin;9. Division of Digestive Diseases, Hepatology, and Nutrition, Connecticut Children’s Medical Center, Hartford, Connecticut;10. Department of Pediatric Gastroenterology, Nationwide Children’s Hospital, The Ohio State University College of Medicine, Columbus, Ohio;11. Department of Pediatrics, The University of Chicago, Chicago, Illinois;12. Department of Pediatrics, University of California at San Francisco, San Francisco, California;13. Department of Gastroenterology and Nutrition, Boston Children’s Hospital, Boston, Massachusetts;14. Department of Pediatrics, University of Utah, Salt Lake City, Utah;15. Department of Pediatrics, Mount Sinai Hospital, New York, New York;16. Department of Pediatrics, Hasbro Children’s Hospital, Providence, Rhode Island;17. Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada;18. The Broad Institute of MIT and Harvard, Cambridge, Massachusetts |
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| Abstract: | Crohn’s disease (CD) and ulcerative colitis (UC), two forms of inflammatory bowel disease (IBD), are chronic, relapsing, and tissue destructive lesions that are accompanied by the uncontrolled activation of effector immune cells in the mucosa. Recent estimates indicate that there are 1.3 million annual cases of IBD in the United States, 50% of which consists of CD and 50% of UC. Chemokines and cytokines play a pivotal role in the regulation of mucosal inflammation by promoting leukocyte migration to sites of inflammation ultimately leading to tissue damage and destruction. In recent years, experimental studies in rodents have led to a better understanding of the role played by these inflammatory mediators in the development and progression of colitis. However, the clinical literature on IBD remains limited. Therefore, the aim of this study was to evaluate systemic concentrations of key chemokines and cytokines in forty-two IBD patients with a range of disease activity compared to levels found in ten healthy donors. We found a significant increase in an array of chemokines including macrophage migration factor (MIF), CCL25, CCL23, CXCL5, CXCL13, CXCL10, CXCL11, MCP1, and CCL21 in IBD patients as compared to normal healthy donors (P < 0.05). Further, we also report increases in the inflammatory cytokines IL-16, IFN-γ, IL-1β and TNF-α in IBD patients when compared to healthy donors (P < 0.05). These data clearly indicate an increase in circulating levels of specific chemokines and cytokines that are known to modulate systemic level through immune cells results in affecting local intestinal inflammation and tissue damage in IBD patients. Blockade of these inflammatory mediators should be explored as a mechanism to alleviate or even reverse symptoms of IBD. |
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| Keywords: | Inflammatory bowel disease (IBD) Chemokine Inflammation Cytokine Ulcerative colitis (UC) Crohn’s disease (CD) |
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