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Titolo:
Interleukin-4 ameliorates crescentic glomerulonephritis in Wistar Kyoto rats
Autore:
Cook, HT; Singh, SJ; Wembridge, DE; Smith, J; Tam, FWK; Pusey, CD;
Indirizzi:
Hammersmith Hosp, Imperial Coll, Sch Med, Dept Histopathol, London W12 0NN, Hammersmith Hosp London England W12 0NN ept Histopathol, London W12 0NN, Hammersmith Hosp, Imperial Coll, Sch Med, Dept Med, London W12 0NN, England Hammersmith Hosp London England W12 0NN ept Med, London W12 0NN, England
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 4, volume: 55, anno: 1999,
pagine: 1319 - 1326
SICI:
0085-2538(199904)55:4<1319:IACGIW>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLOMERULAR PROCOAGULANT ACTIVITY; NITRIC-OXIDE SYNTHASE; TUMOR NECROSIS FACTOR; WKY RATS; ENDOTHELIAL-CELLS; GENE-EXPRESSION; TISSUE FACTOR; MACROPHAGES; NEPHRITIS; RECEPTOR;
Keywords:
macrophage activation; inflammation; glomerular injury; proteinuria; tubulointerstitial scarring;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Cook, HT Hammersmithdonsp, Imperial Coll, Sch Med, Dept Histopathol, Du Cane Rd, Lon Hammersmith Hosp Du Cane Rd London England W12 0NN Cane Rd, Lon
Citazione:
H.T. Cook et al., "Interleukin-4 ameliorates crescentic glomerulonephritis in Wistar Kyoto rats", KIDNEY INT, 55(4), 1999, pp. 1319-1326

Abstract

Background. Activated macrophages play a central role in crescentic glomerulonephritis. Interleukin-4 (IL-4) down-regulates many macrophage proinflammatory activities. We therefore studied the effect of IL-4 on glomerular injury in a model of crescentic glomerulonephritis in the Wistar Kyoto rat. Methods. Glomerulonephritis was induced by i.v. administration of rabbit antirat glomerular basement membrane antiserum (nephrotoxic serum, NTS). In experiment 1, IL-4 was given from two hours before NTS until day 6. In experiment 2, rats were treated from day 0 to 7 and were then monitored until killed on day 28. In experiment 3, IL-4 was given from day 4 to 7. Results. Continuous IL-4 treatment (experiment 1) significantly (P = 0.001) reduced proteinuria (3 +/- 1 mg per 24 hr vs. 56 +/- 7), fibrinoid necrosis (0.06 +/- 0.04 quadrants/glomulus vs. 1.2 +/- 0.1), macrophage infiltration (6.7 +/- 2.6 cells/glom vs. 33 +/- 2.5), CD8+ cells (1.5 +/- 0.6 cells/glom vs. 6.2 +/- 1.1), inducible nitric oxide synthase positive cells (0.04+/- 0.04 cells/glom vs. 3.7 +/- 0.6), proliferating cell nuclear antigen positive cells (3.2 +/- 1 cells/glom vs. 15 +/- 2.3), and glomerular intercellular adhesion molecule-1 expression. Follow-up after seven days of treatment (experiment 2) showed that at four weeks, creatinine clearance was higher in treated rats (1.1 +/- 0.1 ml/min vs. 0.4 +/- 01, P = 0.011), and bothglomerular scarring (P = 0.006) and tubular atrophy (P = 0.006) were less. Delayed treatment (experiment 3) reduced proteinuria (41 +/- 5 mg per 24 hr vs. 97 +/- 9, P = 0.004) and fibrinoid necrosis (0.39 +/- 0.05 quadrants/glom vs. 1.6 +/- 0.1, P - 0.004). There was no difference in macrophage infiltration, but inducible nitric oxide synthase positive cells were reduced (0.6 +/- 0.1 cells/glom vs. 1.8 +/- 0.4, P = 0.01) as were ED3+ cells (0.18+/- 0.06 cells/glom vs. 1.86 +/- 0.21, P = 0.004). Conclusion. In this model of crescentic glomerulonephritis, early IL-4 treatment abolished proteinuria and markedly reduced glomerular inflammation. If treatment was stopped after seven days, there was continuing benefit on glomerular and tubulointerstitial scarring and creatinine clearance at fourweeks. If treatment was delayed until inflammation was established, there was still a reduction of injury, but without an alteration of macrophage numbers, suggesting that IL-4 may be acting, in part, to reduce macrophage activation.

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Documento generato il 01/12/20 alle ore 16:29:26