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In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions
Published on: June 11, 2015
The infectious etiology of vasculitis
Merav Lidar1, Noga Lipschitz, Pnina Langevitz
1Center for Autoimmune Diseases, Rheumatology Unit, Sheba Medical Center (SMC), Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Abstract:
Infectious agents have been implicated in the etiopathogenesis of various vasculitides via numerous and overlapping mechanisms including direct microbial invasion of endothelial cells, immune complex mediated vessel wall damage and stimulation of autoreactive B and/or T cells through molecular mimicry and superantigens. While the causative role of hepatitis B virus in polyarteritis nodosa and hepatitis C virus in mixed cryoglobulinemia is clearly established, evidence for the association of other infectious agents with vasculitis, including human immunodeficiency virus, parvovirus B19, cytomegalovirus, varicella zoster virus, Staphylococcus aureus, rickettsiaceae, Treponema pallidum and Borrelia burgdorferi, among numerous others, is accumulating. The spectrum of association of infectious agents; bacteria, viruses and parasites, with systemic vasculitides, will be reviewed herewith.
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