Podocytes are the major source of IL-1α and IL-1β in human glomerulonephritides

Podocytes are the major source of IL-1α and IL-1β in human glomerulonephritides. To address the question of in situ production of IL-1α and IL-1β in proliferative and non-proliferative forms of human glomerulo-nephritis (GN), we performed immunocytochemical and in situ hybridization studies on renal...

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Hauptverfasser: Niemir, Zofia (VerfasserIn) , Stein, Henning (VerfasserIn) , Dworacki, Grzegorz (VerfasserIn) , Mundel, Peter (VerfasserIn) , Köhl-Hackert, Nadja (VerfasserIn) , Fröhlich, Boris Erwin (VerfasserIn) , Autschbach, Frank (VerfasserIn) , Andrassy, Konrad (VerfasserIn) , Ritz, Eberhard (VerfasserIn) , Waldherr, Rüdiger (VerfasserIn) , Otto, Herwart F. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 1997
In: Kidney international
Year: 1997, Jahrgang: 52, Heft: 2, Pages: 393-403
ISSN:1523-1755
DOI:10.1038/ki.1997.346
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/ki.1997.346
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0085253815601867
Volltext
Verfasserangaben:Zofia I. Niemir, Henning Stein, Grzegorz Dworacki, Peter Mundel, Nadja Koehl, Boris Koch, Frank Autschbach, Konrad Andrassy, Eberhard Ritz, Ruediger Waldherr, Herwart F. Otto

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520 |a Podocytes are the major source of IL-1α and IL-1β in human glomerulonephritides. To address the question of in situ production of IL-1α and IL-1β in proliferative and non-proliferative forms of human glomerulo-nephritis (GN), we performed immunocytochemical and in situ hybridization studies on renal biopsies from patients with mesangial IgA-GN (N = 38), idiopathic membranous GN (MGN; N = 12), minimal change disease (MCD; N = 9), focal segmental glomerulosclerosis (FSGS; N = 5) and acute endocapillary GN (AGN; N = 3). Normal kidneys (N = 10) served as controls. Concomitantly, the expression of IL-1 receptor type I (IL-1 RI), IL-1 receptor type II (IL-1 RII) and of IL-1 receptor antagonist (IL-1 RA) was analyzed. Antibodies against antigens expressed on podocytes (PP-44), endothelial cells (CD31) and monocytes/macrophages (CD11b, CD14, CD68) were applied to attribute the expression of IL-1/IL-1 related peptides to intrinsic glomerular and/or blood-derived infiltrating cells. Our results demonstrate that IL-1 RII is constitutively expressed on endothelial cells, and its expression can be induced in proximal tubular cells and in the interstitium. In diseased glomeruli podocytes are capable of producing IL-1α/β. In MGN and MCD/FSGS, the expression of both IL-1 forms is particularly noted in early stages of the disease and is not only accompanied by a marked reactivity for IL-1 RI, but also for IL-1 RA. In segmental sclerosing lesions in FSGS and in IgA-GN with marked glomerular proliferation and/or sclerosis, a reduced expression of the PP-44 antigen and a diminished ability of podocytes to produce IL-1/IL-1 related peptides are noted. These results suggest that intrinsic glomerular production of IL-1 may be of relevance for the protection of glomeruli from continuing injury. 
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