Etanercept Suppresses Arteritis in a Murine Model of Kawasaki Disease: A Comparative Study Involving Different Biological Agents
Figure 3
Histological observations on the development of vasculitis treated with different biological agents. Arterial inflammation around the aortic root at 2 weeks (a)–(d) and at 4 weeks (e)–(l) treated with IVIG ((a), (e), (i)), etanercept ((b), (f), (j)), methylprednisolone ((c), (g), (k)), and cyclosporine A ((d), (h), (l)). (a) Segmental inflammatory changes were observed in IVIG-treated mice (arrowheads). (b) Rare significant inflammatory changes were observed yet in etanercept-treated mice. (c, d) In methylprednisolone and cyclosporine-A groups, the inflammatory changes were still segmental (arrowheads), and appeared comparable with each other. (e, i) In IVIG-treated mice at 4 weeks, the inflammatory cell infiltration was more pronounced with loss of elastic lamina (arrowheads) extending into the surrounding tissue. (f, j) In the etanercept group at 4 weeks, vascular architecture was almost preserved except for a small segmental inflammatory area (arrowheads). (g, k) In methylprednisolone-treated mice at 4 weeks, the vascular architecture was diffusely distorted or misshapen due to dense inflammatory cell infiltration that expanded into the hear ventricles and connective tissues (arrowheads). (h, l) In cyclosporine-A-treated mice at 4 weeks, the inflammatory cell infiltration was segmental with focal loss of elastic lamina (arrowheads). H&E stain (a)–(h), EMG stain (i)–(l). All images at original magnification of 40. All scale bars: 1 mm.
