Document Detail


Interleukin-6 exacerbates glomerulonephritis in (NZB x NZW)F1 mice.
MedLine Citation:
PMID:  8178944     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The ability of interleukin-6 (IL-6) to modulate immune parameters and mesangial cell function suggests a role for this cytokine in the development of autoimmune glomerulonephritis. This hypothesis was tested in 6-month-old female (NZB x NZW)F1 mice that were administered recombinant human IL-6 (rhIL-6) (50 and 250 micrograms/kg s.c.) for 12 weeks, resulting in an accelerated and severe form of membranoproliferative glomerulonephritis associated with marked upregulation of mesangial major histocompatibility complex class II antigen and glomerular ICAM-1 expression. To distinguish direct effects of rhIL-6 on the renal mesangium from those mediated through the immune system, (NZB x NZW)F1 mice were immunosuppressed with cyclosporin. Immunosuppression by cyclosporin inhibited the development of glomerulonephritis, decreased class II antigen expression, and abrogated IL-6-mediated effects. Administration of neutralizing anti-IL-6 antibody had no effect on the spontaneous development of glomerulonephritis in (NZB x NZW)F1 mice. This finding, together with undetectable IL-6 serum levels, makes a pathogenetic role of endogenously produced IL-6 in this disease model unlikely. In contrast to (NZB x NZW)F1 mice, parental NZW or BALB/c mice given high doses of rhIL-6 (500 micrograms/kg) or recombinant murine IL-6 (100 micrograms/kg) daily for 4 weeks failed to develop morphological or biochemical evidence of glomerulonephritis. Induction of acute phase proteins, anemia, thrombocytosis, and induction of renal class II antigen confirmed the biological activity of IL-6 in these mice. In conclusion, while non-nephritogenic in normal mice, IL-6 accelerates the development of the genetically determined glomerulonephritis of (NZB x NZW)F1 mice through effects mediated by a modulated immune system. Since neutralizing IL-6 antibody treatment did not prevent the development of glomerulonephritis, it is unlikely that increased IL-6 production plays a role in the pathogenesis of lupus nephritis.
Authors:
B Ryffel; B D Car; H Gunn; D Roman; P Hiestand; M J Mihatsch
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of pathology     Volume:  144     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  1994 May 
Date Detail:
Created Date:  1994-06-06     Completed Date:  1994-06-06     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  927-37     Citation Subset:  AIM; IM    
Affiliation:
Institute of Toxicology, Faculty of Medicine, University of Zurich, Switzerland.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / pharmacology
Biological Availability
Cyclosporine / pharmacology
Female
Glomerulonephritis / etiology*,  mortality,  pathology
HLA-D Antigens / drug effects,  metabolism
Interleukin-6 / administration & dosage,  adverse effects*,  antagonists & inhibitors,  metabolism
Male
Mice
Mice, Inbred BALB C
Mice, Inbred NZB
Microscopy, Electron
Proteinuria / etiology
Species Specificity
Survival Rate
Chemical
Reg. No./Substance:
0/Antibodies; 0/HLA-D Antigens; 0/Interleukin-6; 59865-13-3/Cyclosporine
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