AI Article Synopsis
- The study investigates how obesity affects inflammatory arthritis (IA) by creating "fat-free" mice that lack both white and brown fat, leading to unexpected resistance to serum-induced IA despite high neutrophil levels.
- The absence of certain adipokines, particularly adipsin, was found to play a critical role in preventing IA, indicating that fat-derived signals are essential for the disease's development.
- Transplanting wild-type adipose tissue into fat-free mice reinstates their susceptibility to IA, demonstrating that adipose tissue influences immune responses related to arthritis through the production of adipsin.
Article Abstract
We explored the relationship of obesity and inflammatory arthritis (IA) by selectively expressing diphtheria toxin in adipose tissue yielding "fat-free" (FF) mice completely lacking white and brown fat. FF mice exhibit systemic neutrophilia and elevated serum acute phase proteins suggesting a predisposition to severe IA. Surprisingly, FF mice are resistant to K/BxN serum-induced IA and attendant bone destruction. Despite robust systemic basal neutrophilia, neutrophil infiltration into joints of FF mice does not occur when challenged with K/BxN serum. Absence of adiponectin, leptin, or both has no effect on joint disease, but deletion of the adipokine adipsin (complement factor D) completely prevents serum-induced IA. Confirming that fat-expressed adipsin modulates the disorder, transplantation of wild-type (WT) adipose tissue into FF mice restores susceptibility to IA, whereas recipients of adipsin-deficient fat remain resistant. Thus, adipose tissue regulates development of IA through a pathway in which adipocytes modify neutrophil responses in distant tissues by producing adipsin.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6643993 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2019.05.032 | DOI Listing |
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