Evaluation of Th17 pathway in the diagnosis of autosomal dominant polycystic kidney disease.

INTRODUCTION: Current assessment tools of autosomal dominant polycystic kidney disease (ADPKD) diagnosis are challenging. This study evaluated the possible application of assessment of interleukin (IL)-17-related cytokines and the circulatory T helper 17 cells in the diagnosis of ADPKD. MATERIALS AND METHODS: Enrolling 54 ADPKD patients and 54 healthy individuals, we measured serum and urine levels of IL-6, IL-17, IL-23, and transforming growth factor-ß and the peripheral blood frequency of T helper 17 cells through flowcytometry. We computed sensitivity and specificity of each inflammatory marker as well as their different combinations using the receiver operating characteristic curve and discriminant function analysis. RESULTS: The mean serum and urine levels of IL-17 and IL-23 as well as urine levels of IL-6 were higher in ADPKD patients compared to the healthy controls (P < .001). There was no significant difference in the number of T helper 17 cells between the two groups. Among different combinations of the inflammatory markers, the serum IL-17 was the best factor in the diagnosis of ADPKD with a sensitivity as well as specificity of 100%. CONCLUSIONS: It is likely that T helper 17 pathway is involved in the pathogenesis of ADPKD; therefore, it may be beneficial if such a pathway be considered in its diagnosis.

Interleukin-27 and interleukin-23 in patients with systemic lupus erythematosus: possible role in lupus nephritis.

OBJECTIVES: To analyse the concentration of interleukin (IL)-27 and IL-23 in serum and urine of patients with systemic lupus erythematosus (SLE) compared with healthy controls (HC). METHOD: An enzyme-linked immunosorbent assay (ELISA) was used to analyse the serum and urine concentration of IL-27 and IL-23 from 50 patients with lupus nephritis (LN), 55 patients without LN, and 30 HC. The correlations between the levels of IL-27, IL-23, and disease activity, clinical parameters in SLE patients were analysed. RESULTS: The levels of IL-27 and IL-23 increased significantly in the serum and urine of SLE patients with and without LN compared with HC. Moreover, urine levels of IL-27 and IL-23 were correlated with the renal SLE Disease Activity Index (rSLEDAI) score and 24-h urinary protein levels. After 6 months of immunosuppressive treatment, urine IL-27 expression rose significantly in SLE patients with LN. CONCLUSIONS: IL-27 and IL-23 may be involved in the pathogenesis of LN.

IL-17, neutrophil activation and muscle damage following endurance exercise.

The T-cell subset Th17 is induced partly by interleukin (IL)-6 and activated by IL-23, and produces a proinflammatory cytokine IL-17. Since IL-6 increases dramatically following long-lasting endurance exercise, this response may also stimulate the induction of IL-17 and IL-23 after exercise. The aim of this study was to clarify the dynamics of IL-17 in association with endurance exercise-induced muscle damage and inflammatory responses. Fourteen male triathletes participated in a duathlon race consisting of 5 km of running, 40 km of cycling and 5 km of running. Venous blood and urine samples were collected before, immediately after 1.5 h and 3 h after the race. Plasma and urine were analyzed using enzyme-linked immunosorbent assays (ELISA). Haematological and biochemical variables such as neutrophil activation marker (myeloperoxidase: MPO), muscle damage marker (myoglobin: Mb) and soluble receptor activator of nuclear factor (NF)-KB ligand (sRANKL) were also determined to estimate the biological and pathological significance. Plasma concentrations oflL-6 (+26.0x), MPO (+3.2x) and Mb (+4.9x) increased significantly immediately after the race and IL-17 and IL-23 tended to increase. Furthermore, plasma concentrations of IL-12p40 and sRANKL increased significantly after the race. The measured parameters related to Thl 7 cytokines in the urinary output were closely correlated with each other and muscle damage marker. These findings suggest that IL-17 induced by IL-6 and activated by IL-23 or other IL-17 producing-cells and IL-23 might promote neutrophil activation and muscle damage following prolonged endurance exercise.