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Titolo:
Interleukin-11 attenuates nephrotoxic nephritis in Wistar Kyoto rats
Autore:
Lai, PC; Cook, HT; Smith, J; Keith, JC; Pusey, CD; Tam, FWK;
Indirizzi:
Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sch Med, Dept Med,Renal Sect, London W12 0NN, England Univ London Imperial Coll Sci Technol & Med London England W12 0NN gland Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sch Med, Dept Histopathol, London W12 0NN, England Univ London Imperial Coll Sci Technol & Med London England W12 0NN gland Wyeth Genet Inst Inc, Dept Immunol & Hemostasis, Andover, MA USA Wyeth Genet Inst Inc Andover MA USA mmunol & Hemostasis, Andover, MA USA
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 11, volume: 12, anno: 2001,
pagine: 2310 - 2320
SICI:
1046-6673(200111)12:11<2310:IANNIW>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR-KAPPA-B; EXPERIMENTAL CRESCENTIC GLOMERULONEPHRITIS; EXPERIMENTAL AUTOIMMUNE GLOMERULONEPHRITIS; IMMUNE-COMPLEX GLOMERULONEPHRITIS; RECOMBINANT HUMAN INTERLEUKIN-11; NITRIC-OXIDE SYNTHASE; TRANSCRIPTION FACTOR; BASEMENT-MEMBRANE; GLOMERULAR INJURY; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Tam, FWK Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sch Med, Dept Med,Renal Sect, Du Cane Rd, London W12 0NN, England Univ LondonImperial Coll Sci Technol & Med Du Cane Rd London England W12 0NN
Citazione:
P.C. Lai et al., "Interleukin-11 attenuates nephrotoxic nephritis in Wistar Kyoto rats", J AM S NEPH, 12(11), 2001, pp. 2310-2320

Abstract

Interleukin-11 (IL-11) is a multifunctional cytokine with anti-inflammatory activity. The effect of IL-11 was studied in an experimental model of necrotizing glomerulonephritis induced in Wistar Kyoto rats by an injection ofanti-glomerular basement membrane antibody (nephrotoxic serum). Intraperitoneal injection was chosen as the route of IL-11 administration in all experiments. In experiment 1, recombinant human IL-11 (1360 mug) was given 2 h before nephrotoxic serum, then once daily until day 6. In experiment 2, a lower dose of IL-11 (800 mug/d) was used. Rats were treated either with IL-11 400 mug twice daily intraperitoneally or with 800 Ag once daily intraperitoneally for 6 d. In experiment 3, the lower dose of IL-11 was given 2 h before nephrotoxic serum, then twice daily until day 2. In experiment 1, IL-11 significantly reduced proteinuria (13.2 +/- 3.3 versus 63.2 +/- 4.3 mg/24h). fibrinoid necrosis (0.58 +/- 0.08 versus 1.52 +/- 0.06 quadrants/glomerular cross section [gcs]), macrophage infiltration (ED1-positive cells, 24.4 +/- 1.8 versus 39.3 +/- .9 cells/gcs), apoptosis (1.11 +/- 0.1 versus 2.39 +/- 0.2 apoptotic bodies/gcs). and proliferating cell nuclear antigen-positive cells (24.4 +/- 2.0 versus 37.3 +/- 2.3 cells/gcs). Inducible nitricoxide synthase-positive cells were significantly increased (3.1 +/- 0.3 versus 2.0 0.2 cells/gcs). In experiment 2, a lower dose of IL-11 significantly reduced proteinuria and fibrinoid necrosis. Macrophage infiltration was similar in treated and control groups, although the number of sialoadhesin-positive macrophages (ED3+) was significantly reduced in the IL-11-treated rats. In experiment 3, quantitative competitive reverse transcriptase-polymerase chain reaction showed that the mRNA ratio of IL-1 beta/beta -actin inthe treated rats was reduced compared with controls. By the use of probes designed from mouse IL- I I receptor alpha -chain sequence, it was also shown that rat mesangial cells and macrophages expressed IL-11 receptor alpha -chain, demonstrating that they were capable of responding to IL-11. In this model of necrotizing glomerulonephritis, high-dose IL-11 treatment markedly reduced both proteinuria and fibrinoid necrosis. At the lower dose, there was a reduction in glomerular injury and macrophage sialoadhesin expression. but without an alteration of macrophage numbers, suggesting that IL-11 may be acting in part to reduce macrophage activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 11:40:01