A new study describes the mechanistic relationship between the cytokine interleukin-1β, (IL-1β) and obesity, showing that when IL-1β 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-1β, 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.
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-1β in mediating the events leading up to obesity-promoted colorectal cancer. They compared the role of IL-1β 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-1β 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-1β 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.