image: Journal of Interferon & Cytokine Research (JICR) is an authoritative peer-reviewed journal that covers all aspects of interferons and cytokines from basic science to clinical applications.
New Rochelle, NY, October 18, 2018--A new study describes the mechanistic relationship between the cytokine interleukin-1ß, (IL-1ß) and obesity, showing that when IL-1ß levels are increased in obesity, IL-1 receptor signaling activates multiple pathways leading to colon cancer. The study shows that obesity is linked with systemic increases in IL-1ß, activation of Wnt, and proliferation of mouse colon cells, as reported in an article published in Journal of Interferon & Cytokine Research (JICR) from Mary Ann Liebert, Inc., publishers. Click here to read the full-text article free on the Journal of Interferon & Cytokine Research (JICR) website through November 18, 2018.
Joel Mason, Tufts University and Tufts University School of Medicine, Boston MA, and colleagues from Tufts University, coauthored the article entitled "Interleukin-1 Signaling Mediates Obesity-Promoted Elevations in Inflammatory Cytokines, Wnt Activation, and Epithelial Proliferation in the Mouse Colon."
The researchers set out to define the role of IL-1ß in mediating the events leading up to obesity-promoted colorectal cancer. They compared the role of IL-1ß in mice fed either a high-fat (obese) or low-fat (lean) diet. Among the changes they found were that obese mice had 30-80% greater concentrations of IL-1ß in the colonic mucosa, a significant increase in the Wnt signaling cascade, and a significant expansion in the proliferation zone of the colonic crypt.
"This study reveals the close linkage of obesity and the inflammatory response and reflects the broad actions of IL-1ß that define obesity as one of many inflammatory diseases," says Journal of Interferon & Cytokine Research Editor-in-Chief Michael Gale Jr., Department of Immunology, University of Washington, Center for Innate Immunity and Immune Disease.