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Titolo:
SUPPRESSION OF PULMONARY INJURY IN EXPERIMENTAL GOODPASTURES-SYNDROMEBY DEOXYSPERGUALIN (DSP)
Autore:
LAN HY; NIKOLICPATERSON DJ; ZARAMA M; KERR PG; ATKINS RC;
Indirizzi:
MONASH MED CTR,DEPT NEPHROL,246 CLAYTON RD CLAYTON VIC 3168 AUSTRALIA MONASH MED CTR,DEPT NEPHROL CLAYTON VIC 3168 AUSTRALIA
Titolo Testata:
Clinical and experimental immunology
fascicolo: 3, volume: 95, anno: 1994,
pagine: 502 - 508
SICI:
0009-9104(1994)95:3<502:SOPIIE>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR CACHECTIN PLAYS; LYMPHOCYTES-T; CRESCENTIC GLOMERULONEPHRITIS; MONOCLONAL-ANTIBODY; RAT LYMPHOCYTES; KEY ROLE; 15-DEOXYSPERGUALIN; INVIVO; PATHOGENESIS; REJECTION;
Keywords:
DEOXYSPERGUALIN; PULMONARY INJURY; GOODPASTURES SYNDROME; TUMOR NECROSIS FACTOR-ALPHA; IMMUNOSUPPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
H.Y. Lan et al., "SUPPRESSION OF PULMONARY INJURY IN EXPERIMENTAL GOODPASTURES-SYNDROMEBY DEOXYSPERGUALIN (DSP)", Clinical and experimental immunology, 95(3), 1994, pp. 502-508

Abstract

DSP is a potent immunosuppressive drug which can prevent allograft rejection and suppress acute rejection episodes. In this study, the ability of DSP to suppress pulmonary injury in experimental Goodpasture's syndrome was investigated. Passive accelerated anti-glomerular basement membrane (GBM) disease was induced in rats by priming with rabbit IgG, followed 5 days later by injection of rabbit anti-GBM serum (day 0). Groups of five animals were treated with DSP (5 mg/kg intraperitoneally per day) or saline (untreated) from day 0 until being killed on days 1, 7, 14 or 21. At day 1, both DSP-treated and untreated animals exhibited similar pulmonary haemorrhage, oedema, and prominent perivascular leucocyte infiltration. Untreated animals subsequently developed severe widespread pulmonary damage including granulomatous lesions and extensive fibrosis, which correlated with infiltration of macrophages and immune-activated (IL-2R(+)) mononuclear cells (P < 0.01). Tumour necrosis factor-alpha (TNF-alpha), a known mediator of acute lung damage, was produced by pulmonary mononuclear cells throughout the experimental course. In contrast, DSP treatment resolved pulmonary haemorrhage, prevented the appearance of granulomatous lesions, and resulted in ahistologically normal lung structure by day 21. This improvement was associated with a marked suppression of macrophage infiltration (P < 0.001 versus untreated), accumulation of immune activated (IL-2R(+)) mononuclear cells (P < 0.01 versus untreated), and TNF-alpha production (P < 0.05 versus untreated). DSP treatment also suppressed the deposition of rat anti-rabbit IgG immunoglobulin and C3 along the alveolar basement membrane (P < 0.05 versus untreated). In conclusion, DSP suppressed pulmonary injury in accelerated anti-GBM disease by acting on thelocal cellular immune response and the systemic humoral immune response. Further studies are warranted to determine whether this could be auseful drug for the treatment of Goodpasture's syndrome in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 05:58:51