Inflammatory Profiling of Peripheral Arterial Disease

The progression of peripheral arterial disease (PAD) is poorly understood but may be caused by an underlying in. ammatory dysfunction. This study therefore pro. led interleukin (IL)-1 beta, IL-2, IL4, IL-6, IL-8, IL-10, IL-13, anticardiolipin, and anti-beta 2-glycoprotein 1 antibody concentrations and characterized patients' in. ammatory response in vitro. Patients were classified according to World Health Organization criteria and ankle-brachial pressure index into critical ischemics (n = 20), stable claudicants (n = 20), and controls (n = 20). In vitro studies involved culturing whole blood with RPMI-1640 for 24 hr with and without 1 mu g/mL lipopolysaccharide and pro. ling cytokine production. Autoantibody levels were measured using enzyme-linked immunosorbent assays, while cytokine profiles were determined by multiplex immunoassay. Serum IL-6, IL-10, IL-13, and anti-beta 2-glycoprotein 1 antibody levels were higher in PAD (p < 0.05). In the case of IL-6 and anti-beta 2-glycoprotein 1 antibody, levels reflected increasing disease severity (p < 0.05). In vitro studies revealed that IL-8 and IL-13 secretory capacities were significantly higher in PAD after 6 hr. However, when these were standardized against patient leukocyte count, cytokine production profiles did not differ. PAD features an increased in. ammatory burden irrespective of Th1:Th2 cytokine type; this is more pronounced with increasing disease severity. However, the in. ammatory hyperresponsiveness of cultured whole blood from PAD patients probably relates to associated leukocytosis, rather than being attributable to an inherent in. ammatory dysfunction.