[Tuberculosis in a Parisian internal medicine hospital unit. 50 cases].
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AIDS-Related Opportunistic Infections↗
Biomedical subjects
C Haas
Publications and source records attributed to C Haas.
Lipopolysaccharide-induced glomerulonephritis develops in the absence of interferon-gamma signaling.
IFN gamma is a costimulator of macrophage activation and it plays an important role as a proinflammatory cytokine by upregulation of adhesion molecules and MHC antigens. In this study we tested the role of IFN gamma in a model of endotoxin-induced glomerulonephritis. A systemic lupus-like disease was induced by injection of 50 micrograms bacterial LPS twice a week for 4 weeks in wild-type and in IFN gamma receptor-deficient (IFN gamma R-/-) mice. The renal cortex was examined by immunofluorescence and by light microscopy. LPS treatment induced an increase in serum levels of IgG and anti-dsDNA antibodies. A mild glomerulonephritis was characterized morphologically, but proteinuria was not observed. The main histological features of glomerulonephritis were an increase in ICAM-1 expression, deposition of immune complexes and of complement in the glomeruli, increased mesangial matrix and mesangial hypercellularity. The number of intraglomerular leukocytes, detected by MHC class-II and LFA-1 expression increased roughly 4-fold. All those alterations took place in a similar manner in wild-type and in IFN gamma R-/-mice. Therefore it is concluded that IFN gamma does not play an important role in the development of endotoxic glomerulonephritis.
Animals↗
Crescentic glomerulonephritis in interferon-gamma receptor deficient mice.
Activation of macrophages by T cells is considered an initiating event in glomerular crescent formation. Since interferon-gamma (INF gamma) is a key mediator in T-cell-mediated activation of macrophages, we decided to test its role in a model of crescentic glomerulonephritis. An anti-glomerular basement membrane (GBM) serum was injected intravenously in presensitized wild-type or IFN gamma receptor deficient (IFN gamma(R)-/-) mice. Glomerulonephritis with glomerular crescents and tubulointerstitial inflammation developed in both strains, even though most evaluated morphological parameters and proteinuria indicated a less severe pathology in the mutant mice compared to the wild type. Thus, IFN gamma is not essential either for glomerular crescent formation or for tubulointerstitial involvement in anti-GBM glomerulonephritis in mice. In conclusion, the role of macrophages in this model might have been overestimated, or other cytokines may compensate for deficient IFN gamma signaling in the activation of macrophages.
Animals↗