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- Title
Podocytes are the major source of IL-1α and IL-1β in human glomerulonephritides.
- Authors
Niemir, Zofia I.; Stein, Henning; Dworacki, Grzegorz; Mundel, Peter; Koehl, Nadja; Koch, Boris; Autschbach, Frank; Andrassy, Konrad; Ritz, Eberhard; Waldherr, Ruediger; Otto, Herwart F.
- Abstract
To address the question of <em>in situ</em> production of IL-1α and IL-1β in proliferative and non-proliferative forms of human glomerulonephritis (GN), we performed immunocytochemical and <em>in situ</em> hybridization studies on renal biopsies from patients with mesangial IgA-GN (<em>N</em> = 38), idiopathic membranous GN (MGN; <em>N</em> = 12), minimal change disease (MCD; <em>N</em> = 9), focal segmental glomerulosclerosis (FSGS; <em>N</em> = 5) and acute endocapillary GN (AGN; <em>N</em> = 3). Normal kidneys (<em>N</em> = 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.
- Subjects
IMMUNOGLOBULINS; CLINICAL pathology; URINARY organs; LEUCOCYTES; KILLER cells; PEPTIDES
- Publication
Kidney International, 1997, Vol 52, Issue 2, p393
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/ki.1997.346