Figure 3

IL-6-deficiency rescues phenotypes seen in hIL-1α cTg mice. hIL-1 cTg (cTg) mice were crossed with IL-6-deficient (IL-6 KO) mice to yield cTg/IL-6 KO mice. PolyI-PolyC was injected into eight-week-old Ctl, cTg or cTg/IL-6 KO mice, and ankle thickness measured at indicated time points (a). Data represent mean ankle thickness ± SD (n = 3 for control; n = 3 for cTg mice; n = 8 for cTg+IL-6 KO; ^*P < 0.05, ^**P < 0.01, NS not significant, cTg vs cTg/IL-6 KO). Three weeks after PolyI-PolyC injection, ankle joints (b–d) and peripheral blood (e) were collected from each mouse. Ankle tissue specimens from all three genotypes were stained with HE (upper panels) or safranin O and methyl green (lower panels) (b), the safranin O-positive articular cartilage area was scored (b) and Mankin scores were evaluated (c). Data in (b,c) represent mean safranin O-positive area (b) (n = 3 for control; n = 3 for cTg mice; n = 3 for cTg+IL-17 KO mice; ^**P < 0.01, NS not significant) or Mankin score (c) ± SD (n = 3 for control; n = 3 for cTg mice; n = 3 for cTg/IL-6 KO mice; ^*P < 0.05, NS not significant). Bar, 100 µm. Destruction of ankle bone in Ctl, cTg or cTg/IL-6 KO mice was evaluated by micro-CT (d). White blood cell (WBC), hemoglobin (Hb) and platelet (Plt) counts in peripheral blood were determined and are shown as mean indicated parameter ± SD (e) (n = 6 for control; n = 3 for cTg mice; n = 8 for cTg+IL-6 KO; ^*P < 0.05, NS not significant).