Gastrointestinal Vasculitis in Autoimmune-Prone (NZW × BXSB)F 1 Mice: Association with Anticardiolipin Autoantibodies

Abstract

Abstract

Gastrointestinal vasculitis is a fatal aspect of systemic lupus erythematosus. Whether lupus-prone strains of mice develop gastrointestinal vasculitis, and whether it is accompanied by elevated titres of anticardiolipin autoantibody is not known. Lupus-prone (NZW × BXSB)F₁ (W/BF₁) mice, and other strains were examined immunohistologically. Levels of anticardiolipin autoantibody and circulating immune complexes were determined by microELISA. Reciprocal haploidentical marrow transplantations between W/BF₁ and autoimmune-resistent B6C3F₁ mice were made. Young adult W/BF₁ mice had the highest incidence of gastrointestinal vasculitis (61%), and the highest mean titre of anticardiolipin autoantibody. Lesions consisted of subintimal fibrinoid degeneration in arterioles of the duodenum, jejunum and ileum, and were prevented, or alternatively induced by reciprocal marrow transplantations between W/BF₁ and B6C3F₁ mice. Mice engrafted with W/BF₁ marrow which developed vasculitis had higher titres of anticardiolipin autoantibodies than engrafted mice free of vasculitis (P < 0.005). This represents the first report of gastrointestinal vasculitis as an aspect of systemic autoimmunity in lupus-prone mice. The concurrent elevation of anticardiolipin autoantibody and development of vasculitis suggests that anticardiolipin autoantibodies, and their proposed thrombogenic and vascular injury consequences, contribute to development of microvasculitis in lupus-prone mice.