Decreased IL-10 mRNA expression in patients with advanced renal failure undergoing conservative treatment.
Chronic renal failure (CRF) is characterized by persistent systemic inflammatory response. We tested the hypothesis that the balance between synthetic capacity of pro-inflammatory, as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, and anti-inflammatory cytokines, as IL-10, may become progressively impaired during decline of renal function. Cytokine mRNA transcript levels (fraction of GAPDH mRNA) were detected by real time RT-PCR technique in whole blood cells of patients with far-advanced or less-advanced CRF (glomerular filtration rate lower or greater than 15ml/min per 1.73m(2), respectively) undergoing conservative treatment and in healthy controls. TNF-alpha mRNA levels were greater (p<0.05) in the patients with far-advanced CRF than in those with less-advanced CRF. IL-6 mRNA levels were not significantly different in the two groups. Both groups of patients exhibited greater (p<0.05) TNF-alpha and IL-6 mRNA levels than the healthy controls. IL-10 mRNA levels were greater (p<0.05) in the patients with less-advanced CRF (65+/-18) than in the healthy controls (12+/-2). Nonetheless, in the patients with far-advanced CRF, IL-10 mRNA levels (20+/-10) were lower (p<0.05) than in the patients with less-advanced CRF and not significantly different than in the healthy controls. In conclusion, advanced renal failure is characterized by unbalanced synthetic capacity of pro- and anti-inflammatory cytokines. A progressive decrease in IL-10 synthetic capacity during the course of CRF could contribute to increasing cardiovascular risk.
Bosutti
Alessandra
A
Department of Clinical, Morphological and Technological Sciences, Division of Internal Medicine, University of Trieste, Clinica Medica, Ospedale di Cattinara, Strada di Fiume 447, 34149 Trieste, Italy.
Grassi
Gabriele
G
Fiotti
Nicola
N
Guarnieri
Gianfranco
G
Biolo
Gianni
G
D000368:Aged; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009133:Muscular Atrophy / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D012333:RNA, Messenger / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
C508609:IL10 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10