The etiology of ANCA-associated vasculitis is unknown. Currently, it is believed that disease may be triggered by infection with the release of proinflammatory cytokines in genetically susceptible individuals. Priming of PMNs and endothelial cells by these cytokines allows ANCAs to activate PMNs, with damage localized to the endothelium, resulting in early lesions. Damage and activation of endothelial cells produces proinflammatory chemokines and cytokines with influxes of monocytes and T cells that intensify endothelial damage. In the kidney, these changes eventually lead to crescent formation. Antigen-specific memory T cells persist after disease remission with the potential of reactivation and disease relapse. Although our understanding of the pathophysiologic mechanisms of ANCA-associated vasculitis is far greater now than when ANCAs were first identified in 1982, more experimental work in combination with clinical observations is required to further elucidate these mechanisms.
"Recently, there have been many reports suggesting a relationship with microbial infection or antigens and vascular disease. There are reports to suggest the participation of ANCA-associated vasculitis and infection . In addition, research into the mechanisms of innate immunity in response to infectious diseases has advanced rapidly. "
[Show abstract][Hide abstract] ABSTRACT: It was reported previously that a Candida albicans water-soluble fraction (CAWS), including a mannoprotein and β-glucan complex, has strong potency in inducing fatal necrotizing arteritis in DBA/2 mice. In this study, histopathological changes and cardiac function were investigated in this system. One mg/day of CAWS was given to DBA/2 mice via peritoneal injection for five days. The CAWS-treated DBA/2 mice were induced aortitis and died at an incidence of 100% within several weeks. Histological findings included stenosis in the left ventricular outflow tract (LVOT) and severe inflammatory changes of the aortic valve with fibrinoid necrosis. Cardiomegaly was observed and heart weight increased 1.62 fold (P < 0.01). Echocardiography revealed a severe reduction in contractility and dilatation of the cavity in the left ventricle (LV): LV fractional shortening (LVFS) decreased from 71% to 38% (P < 0.01), and the LV end-diastolic diameter (LVDd) increased from 2.21 mm to 3.26 mm (P < 0.01). The titer of BNP mRNA increased in the CAWS-treated group. Severe inflammatory changes resulting from CAWS brought about lethal LV dysfunction by aortic valve deformation with LVOT stenosis. This system is proposed as an easy and useful experimental model of heart failure because CAWS arteritis can be induced by CAWS injection alone.
International journal of vascular medicine 07/2012; 2012:570297. DOI:10.1155/2012/570297
[Show abstract][Hide abstract] ABSTRACT: The vasculitides are a heterogeneous group of diseases that are characterized by blood vessel inflammation and necrosis. They have a wide spectrum of manifestations due to the involvement of arteries and other vessels of various sizes and locations. Classification criteria are useful in improving our understanding of the epidemiology of these conditions but they are not diagnostic criteria. In recent years a progressive increase in incidence has been reported. Both giant cell arteritis and Wegener's granulomatosis are more common in the Northern hemisphere. Environmental factors have been implicated in the pathogenesis of these syndromes. Recent studies in patients with large and small-sized vasculitides support a genetic influence in disease susceptibility. They have confirmed the association of giant cell arteritis and Henoch-Schönlein purpura with HLA-DRB1 alleles. Moreover, the polymorphisms of other genes, such as interleukin-1 receptor antagonist, seem to be implicated in disease severity in patients with cutaneous vasculitis.
Bailliè re s Best Practice and Research in Clinical Rheumatology 01/2003; 16(5):833-45. DOI:10.1053/berh.2002.0260 · 2.60 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Anti-neutrophil cytoplasm antibody associated vasculitides are autoimmune diseases that require treatment with powerful immunosuppressants in order to avert life threatening complications, principally renal failure and lung haemorrhage. Their pathogenesis remains unclear but the circulating autoantibodies are almost certainly instrumental in mediating vascular inflammation. Recent insights into leukocyte-autoantibody interactions support this assertion and may direct future therapeutic strategies, perhaps circumventing some of the toxicity associated with currently used drugs.
The International Journal of Biochemistry & Cell Biology 04/2003; 35(3):277-82. DOI:10.1016/S1357-2725(02)00094-8 · 4.05 Impact Factor
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