biostudies-literatureUnknown3(1)O'Neill L<h4>Objective</h4>The aim of this study was to examine the pro-inflammatory effects of IL-6 in <i>ex vivo</i> temporal artery explant cultures.<h4>Methods</h4>Patients meeting 1990 ACR classification criteria for GCA were prospectively recruited. Temporal artery biopsies were obtained and temporal artery explants cultured <i>ex vivo</i> with IL-6 (10-40 ng/ml) in the presence or absence of its soluble receptor (sIL-6R; 20 ng/ml) for 24 h. Explant supernatants were harvested after 24 h and assayed for IFN-γ, TNF-α, Serum amyloid A, IL-1β, IL-17, IL-8, angiotensin II and VEGF by ELISA. Myofibroblast outgrowths, cytoskeletal rearrangement and wound repair assays were performed.<h4>Results</h4>IL-6 augmented production of VEGF, but not of any of the other pro-inflammatory mediators assayed. No differences were observed in the explants cultured in the presence or absence of the sIL-6R or between those with a positive (<i>n</i> = 11) or negative (<i>n</i> = 17) temporal artery biopsy. IL-6 did not enhance myofibroblast proliferation or migration. Western blot analysis confirmed signalling activation, with increased expression of pSTAT3 in response to IL-6+sIL-6R.<h4>Conclusion</h4>IL-6 stimulation of temporal artery explants from patients with GCA neither increased expression of key pro-inflammatory mediators nor influenced myofibroblast proliferation or migration.Rheumatology advances in practicerkz011https://www.ebi.ac.uk/biostudies/studies/S-EPMC6649906biostudies-literatureInterleukin-6 does not upregulate pro-inflammatory cytokine expression in an <i>ex vivo</i> model of giant cell arteritis.PMC6649906O'Neill LMolloy ESMcCormick JGao WMcCarthy GMVeale DJMurphy CCFearon UfalseInterleukin-6 does not upregulate pro-inflammatory cytokine expression in an <i>ex vivo</i> model of giant cell arteritis.<h4>Objective</h4>The aim of this study was to examine the pro-inflammatory effects of IL-6 in <i>ex vivo</i> temporal artery explant cultures.<h4>Methods</h4>Patients meeting 1990 ACR classification criteria for GCA were prospectively recruited. Temporal artery biopsies were obtained and temporal artery explants cultured <i>ex vivo</i> with IL-6 (10-40 ng/ml) in the presence or absence of its soluble receptor (sIL-6R; 20 ng/ml) for 24 h. Explant supernatants were harvested after 24 h and assayed for IFN-γ, TNF-α, Serum amyloid A, IL-1β, IL-17, IL-8, angiotensin II and VEGF by ELISA. Myofibroblast outgrowths, cytoskeletal rearrangement and wound repair assays were performed.<h4>Results</h4>IL-6 augmented production of VEGF, but not of any of the other pro-inflammatory mediators assayed. No differences were observed in the explants cultured in the presence or absence of the sIL-6R or between those with a positive (<i>n</i> = 11) or negative (<i>n</i> = 17) temporal artery biopsy. IL-6 did not enhance myofibroblast proliferation or migration. Western blot analysis confirmed signalling activation, with increased expression of pSTAT3 in response to IL-6+sIL-6R.<h4>Conclusion</h4>IL-6 stimulation of temporal artery explants from patients with GCA neither increased expression of key pro-inflammatory mediators nor influenced myofibroblast proliferation or migration.2019-01-01T00:00:00Z20192024-02-15T08:19:56.44Z2019-08-24T07:01:51ZS-EPMC66499063143199910.1093/rap/rkz011