Résumé
Autoimmune diseases might be caused by an imbalance of T-helper cell [Th] cytokines. Lupus nephritis [LN] is dominated by a Th1 immune response in systemic lupus erythematosus [SLE]. Interleukin-18 [IL-18] promotes polarization of the immune response towards Th1 in LN. Nitric oxide [NO] is involved in the pathogenesis of glomerulonephuitis and collagen-vascular diseases. The aim of the present study is to investigate role of IL-18 and NO in patients with LN and to study the correlation between them and Systemic Lupus Erythematosus Disease Activity Index [SLEDAI] score and whether these two molecules are associated with renal involvement in patients with SLE. We investigated plasma concentrations of IL-18 and NO and gene expression of IL-18 was analyzed by Reverse transcription-polymerase chain reaction [RT-PCR] in 19 SLE patients with LN, [group1] and 15 SLE patients without renal involvement [group2] and 15 age- and sex-matched healthy control subjects [group3]. IL-18 and NO concentrations were measured by ELISA and colourimetric non-enzymatic assay, respectively. Plasma IL-18 and NO concentrations were significantly higher in renal group 1 than non renal group 2 and normal control group 3 [p=0.001 and 0.01 respectively]. Elevation of plasma IL-18 in renal group 1 correlated positively with SLE disease activity index and plasma NO concentration [r=0.35, p=0.0001 and r= 0.46, P=0.01, respectively], and the latter also showed a positive correlation with serum creatinine [r=0.69, P=0.001] and urea [r = 0.28, P = 0.001]. There was no significant difference in gene expressions of IL-18 in peripheral blood mononuclear cells among renal group 1, non renal group 2 and normal control group3. IL-18 is therefore suggested to play a crucial role in the inflammatory processes of renal disease in SLE. IL-18 may play a crucial role in the inflammatory process of renal disease in SLE and its measurement may be helpful for the early identification of lupus patients with LN. Elevated concentrations of circulating NO can serve as indicators of endothelial activation and/or damage, which may occur in the pathogenesis of SLE with LN