Background Systemic vasculitides include a heterogeneous group of clinical syndromes characterised by inflammation and necrosis of blood vessel walls. Any type of vessels throughout the body may be involved with protean clinical manifestations, and pathogenetic mechanisms remain mainly unknown.
Objectives Aim of our study was to test the hypothesis that chemokines, cytokines, and eosinophilic inflammation markers could be involved in systemic vasculitides pathogenetic process.
Methods We studied 19 patients with systemic vasculitides diagnosed according to ACR 1990 criteria: 7 pts. with Churg-Strauss vasculitide (CS), 7 pts. with Wegener’s Granulomatosis (GW), 5 pts. with Panarteritis Nodosa (PAN) and 24 normal healthy subjects (NHS) as controls. Serum levels of the following mediators: macrophage inflammatory protein 1α (MIP1α), monocyte chemotactic protein 1 (MCP1), RANTES, interleukin 5 (IL5), granulocyte macrophage-colony stimulating factor (GM-CSF) and eosinophil cationic protein (ECP) were tested by ELISA. For the statistical analysis U-Mann Whitney test has been used.
Results Among chemokines, serum levels of MCP1and RANTES were significantly higher in systemic vasculitides than NHS (p < 0.001 and p < 0.007 respectively), while no differences were demonstrated in MIP1α serum levels. Regarding cytokines studied, IL5 and GM-CSF serum levels were significantly higher in systemic vasculitides than NHS (p < 0.001). Also ECP serum levels resulted increased in systemic vasculitides than NHS (p < 0.04) with a significative correlation between ECP levels and blood eosinophilia in vasculitides patients. Furthermore, a specific subgroup analysis showed that serum levels of RANTES, IL5, and ECP resulted increased mainly in CS and GW, while MCP1 and GM-CSF mainly in CS and PAN.
Conclusion Our study demonstrate the increased production of chemokines and cytokines in systemic vasculitides patients. Moreover, the finding of higher ECP serum levels in our patients induce us to hypothesise that eosinophils are actively involved in vasculitides etiopathogenesis.
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