Elevated levels of Interleukin (IL)-33 induce bone pathology but absence of IL-33 does not negatively impact normal bone homeostasis

Cytokine
Angela J OkraglyRobert J Benschop

Abstract

Interleukin (IL)-33 is a member of the IL-1 family. IL-33 effects are mediated through its receptor, ST2 and IL-1RAcP, and its signaling induces the production of a number of pro-inflammatory mediators, including TNFα, IL-1β, IL-6, and IFN-γ. There are conflicting reports on the role of IL-33 in bone homeostasis, with some demonstrating a bone protective role for IL-33 whilst others show that IL-33 induces inflammatory arthritis with concurrent bone destruction. To better clarify the role IL-33 plays in bone biology in vivo, we studied IL-33 KO mice as well as mice in which the cytokine form of IL-33 was overexpressed. Mid-femur cortical bone mineral density (BMD) and bone strength were similar in the IL-33 KO mice compared to WT animals during the first 8months of life. However, in the absence of IL-33, we observed higher BMD in lumbar vertebrae and distal femur in female mice. In contrast, overexpression of IL-33 resulted in a marked and rapid reduction of bone volume, mineral density and strength. Moreover, this was associated with a robust increase in inflammatory cytokines (including IL-6 and IFN-γ), suggesting the bone pathology could be a direct effect of IL-33 or an indirect effect due to the induction of other mediator...Continue Reading

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Citations

Apr 6, 2016·AIDS·Vikram MehrajUNKNOWN Montreal Primary HIV Infection, the Canadian Long-Term Non-Progressors Study Groups
Oct 9, 2019·Technology and Health Care : Official Journal of the European Society for Engineering and Medicine·Yu-Hang GaoXin Qi
Feb 20, 2020·International Journal of Molecular Sciences·Massimo De MartinisLia Ginaldi
Jan 26, 2021·Frontiers in Immunology·Massimo De MartinisSebastiano Gangemi

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