Neutrophil attractant protein-1 interleukin 8 and its autoantibodies in IgA nephropathy

Human neutrophil attractant protein-1/interleukin 8 (IL-8) has been shown to activate neutrophils to degranulate in vitro and to be a potent chemotactic agonist for neutrophils and lymphocytes in vitro and in vivo. There is accumulating evidence that neutrophils are involved in inflammatory injury in IgA nephropathy (IgAN). We studied the serum levels of IL-8 and its autoantibodies of the IgA or IgG class in 36 patients with IgAN in comparison with 31 healthy controls and 26 patients with other primary glomerulonephritides (CGN). Interleukin 8 was more frequently detected in sera of patients with IgAN and their serum levels were significantly higher than those of healthy controls. The free IL-8 autoantibodies of the IgA, but not IgG class, were more frequently detected in patients with IgAN and their serum levels were significantly elevated compared with both groups of controls. The complexed IL-8 autoantibodies of either class were not different among the three groups of subjects. Again the ratio of free to complexed IL-8 autoantibodies of the IgA class was raised in patients with IgAN. Histologic examination revealed increased polymorphs and monocyte/macrophage infiltration in IgAN compared with other glomerulonephritides. When the serum levels of IL-8 and IL-8 autoantibodies were compared between IgAN patients with milder pathology and those with more severe pathology, the latter group had significantly higher serum levels of free and complexed IL-8 autoantibodies of the IgA class. These observations suggest a possible role for IL-8 and its autoantibodies of the IgA class in the inflammatory process of IgAN. These autoantibodies may provide a clinically useful marker for the diagnosis of disease severity.