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Arthritis Research (1)
Journal of Clinical Investigation (1)
Hillebrands, Jan-Luuk (1)
Kallenberg, Cees GM (1)
Klatter, Flip A. (1)
Nieuwenhuis, Paul (1)
Popa, Eliane R (1)
Popa, Eliane R. (1)
Rozing, Jan (1)
Stegeman, Coen A (1)
Willem Cohen Tervaert, Jan (1)
van den Hurk, Bart M.H. (1)
Year of Publication
Staphylococcus aureus and Wegener's granulomatosis
Stegeman, Coen A
Kallenberg, Cees GM
Willem Cohen Tervaert, Jan
Wegener's granulomatosis (WG) is a form of systemic vasculitis. It is characterized by granulomatous inflammation in the upper and lower airways, vasculitis and necrotizing glomerulonephritis, and is strongly associated with antineutrophil cytoplasmic antibodies against proteinase 3. Since the etiology of the disease is not clear, treatment, consisting of corticosteroids and immunosuppressives, is nonspecific and associated with severe side effects. Pinpointing the trigger(s) of the disease would highly improve treatment. Clinical evidence shows that an infectious agent, the bacterium Staphylococcus aureus, is a risk factor for disease relapse, suggesting its involvement in the pathogenesis of WG. Here we review both clinical and experimental data that either indicate or support a role for S. aureus in WG.
autoimmunity; co-trimoxazole; Staphylococcus aureus; superantigens; Wegener's granulomatosis
Origin of neointimal endothelium and α-actin–positive smooth muscle cells in transplant arteriosclerosis
Klatter, Flip A.
van den Hurk, Bart M.H.
Journal of Clinical Investigation
The development of transplant arteriosclerosis (TA) is today’s most important problem in clinical organ transplantation. Histologically, TA is characterized by perivascular inflammation and progressive intimal thickening. Current thought on this process of vascular remodeling assumes that neointimal vascular smooth muscle (VSM) cells and endothelium in TA are graft-derived, holding that medial VSM cells proliferate and migrate into the subendothelial space in response to signals from inflammatory cells and damaged graft endothelium. Using MHC class I haplotype-specific immunohistochemical staining and single-cell PCR analyses, we show that the neointimal α-actin–positive VSM cells in rat aortic or cardiac allografts are of recipient and not of donor origin. In aortic but not in cardiac allografts, recipient-derived endothelial cells (ECs) replaced donor endothelium. Cyclosporine treatment prevents neointima formation and preserves the vascular media in aortic allografts. Recipient-derived ECs do not replace graft endothelium after cyclosporine treatment. We propose that, although it progresses beyond the needs of functional repair, TA reflects the activity of a normal healing process that restores vascular wall function following allograft-induced immunological injury.
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