Increased release of tumor necrosis factor-alpha by monocytes from patients with glomerulonephritis.
The release of tumor necrosis factor-alpha (TNF) was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from patients with glomerulonephritis (GN) and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced TNF release were significantly higher in PBM isolated from patients with IgA nephropathy (IgA N) and membranous nephropathy (MN) as compared to normal controls. These biological activities were neutralized by a specific antibody to TNF. In patients with IgA N and MN TNF levels did not correlate with clinical disease activity. We conclude that in vitro GN PBM are hyperactive in their release of TNF, and that this enhanced release of TNF in vitro may reflect a secondary consequence of monocyte activation rather than a primary cellular defect in GN.
Matsumoto
K
K
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
D000328:Adult; D005260:Female; D005921:Glomerulonephritis / Q000097:blood / Q000378:metabolism*; D005922:Glomerulonephritis, IGA / Q000378:metabolism; D015433:Glomerulonephritis, Membranous / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007963:Leukocytes, Mononuclear / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000502:physiology; D008297:Male; D009402:Nephrosis, Lipoid / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D014409:Tumor Necrosis Factor-alpha