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Abstract
The erosion and breakdown of cartilage is generally recognized to be an integral manifestation of arthritic disease, which is often accompanied by the development and progression of inflammation associated with it. Commercial shark cartilage (SC) is a popular dietary supplement taken for the prevention and/or control of chronic disease, including arthritis. The efficacy of SC in maintaining joint health remains questionable; there is a lack of sufficient reliable information on its effect on immunocompetent cells, and the potential health risks involved have not been adequately assessed. Our earlier in vitro studies showed that SC extracts induce a Th1-type inflammatory cytokine response in human leucocytes, and collagen type II alpha 1 protein was shown to be an active cytokine-inducing component in SC. In this study, we further define the cellular response to SC stimulation by classifying leucocytes into primary and secondary responders employing enriched leucocyte subpopulations. Inhibitors of specific signaling pathways were used to verify the functional effect of SC on specific pathway(s) utilized. Results indicate the monocyte/macrophage as the initially responding cell, followed by lymphocytes and the production of interferon-γ. Chemokines, MCP-1 and RANTES, were produced at significant levels in stimulated leucocyte cultures. Initial cellular activation is likely followed by activation of Jun Kinase and p38 mitogen-activated protein kinase signal transduction pathways. This study presents evidence of significant immunological reactivity of components of commercial SC supplement, which could pose a potential health risk for consumers, particularly those with underlying inflammatory disease such as irritable bowel syndrome and arthritis.
Acknowledgements
The authors thank volunteers who donated blood and the Comparative Immunology core laboratory for use of equipment. The protocol for the collection and isolation of leucocytes from peripheral blood of healthy human donors was approved by FIU’s Institutional Review Board (IRB).
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.
L. M. nor S. L. S. are associated with the manufacturers of commercial shark cartilage.
This study was supported, in part, by a summer research award to L. M. (NIH/NIGMS R25 GM061347) and a Faculty Research Enhancement Award to S. L. S. funded by the NICHD/EARDA program (G11HD038341).
Author contributions
L. M. and S. L. S. contributed equally in different ways to the design, development and support of this study, the analysis and interpretation of data and the preparation of this manuscript.
