Interleukin-1 production by lipopolysaccharide-stimulated glomeruli from rats with nephrotoxic serum nephritis. 1989

K Matsumoto
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

The objective of the present work was to characterize some aspects of interleukin-1 (IL-1) production by nephritic glomeruli after stimulation with bacterial lipopolysaccharide (LPS). Freshly isolated glomeruli from rats with an accelerated autologous form of nephrotoxic serum nephritis (NTSN) were incubated for 24 h in the presence of LPS. The modified NTSN was produced by an intravenous injection of nephrotoxic serum (NTS) into the rats which had been previously immunized with rabbit IgG and Freund's complete adjuvant. The glomerular cultures of the NTSN rats were found to release significantly increased amounts of IL-1 after LPS stimulation when compared to the values obtained with normal controls and the other control group, consisting of preimmunized rats (rabbit IgG), then given normal rabbit globulin instead of NTS. To block the effect of prostaglandins on the IL-1 assay, we cultured the glomeruli with the addition of indomethacin and assayed IL-1 activity in the culture supernatants. The use of indomethacin resulted in a further increase in IL-1 production. The administration of a rabbit anti-rat macrophage serum reduced the production of IL-1 activity in the NTSN rats. Our findings support the notion that at least in NTSN rats activated macrophages are present and probably account for their increased IL-1 activity. This description of IL-1 activity produced by LPS-stimulated nephritic glomeruli may introduce a new element to the early events leading to glomerular inflammation.

UI MeSH Term Description Entries
D007116 Immunization, Passive Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER). Convalescent Plasma Therapy,Immunoglobulin Therapy,Immunotherapy, Passive,Normal Serum Globulin Therapy,Passive Antibody Transfer,Passive Transfer of Immunity,Serotherapy,Passive Immunotherapy,Therapy, Immunoglobulin,Antibody Transfer, Passive,Passive Immunization,Therapy, Convalescent Plasma,Transfer, Passive Antibody
D007213 Indomethacin A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES. Amuno,Indocid,Indocin,Indomet 140,Indometacin,Indomethacin Hydrochloride,Metindol,Osmosin
D007375 Interleukin-1 A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. IL-1,Lymphocyte-Activating Factor,Epidermal Cell Derived Thymocyte-Activating Factor,Interleukin I,Macrophage Cell Factor,T Helper Factor,Epidermal Cell Derived Thymocyte Activating Factor,Interleukin 1,Lymphocyte Activating Factor
D007678 Kidney Glomerulus A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue. Glomerulus, Kidney
D008070 Lipopolysaccharides Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed) Lipopolysaccharide,Lipoglycans
D008262 Macrophage Activation The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants. Activation, Macrophage,Activations, Macrophage,Macrophage Activations
D008264 Macrophages The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.) Bone Marrow-Derived Macrophages,Monocyte-Derived Macrophages,Macrophage,Macrophages, Monocyte-Derived,Bone Marrow Derived Macrophages,Bone Marrow-Derived Macrophage,Macrophage, Bone Marrow-Derived,Macrophage, Monocyte-Derived,Macrophages, Bone Marrow-Derived,Macrophages, Monocyte Derived,Monocyte Derived Macrophages,Monocyte-Derived Macrophage
D008297 Male Males
D011919 Rats, Inbred Strains Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding. August Rats,Inbred Rat Strains,Inbred Strain of Rat,Inbred Strain of Rats,Inbred Strains of Rats,Rat, Inbred Strain,August Rat,Inbred Rat Strain,Inbred Strain Rat,Inbred Strain Rats,Inbred Strains Rat,Inbred Strains Rats,Rat Inbred Strain,Rat Inbred Strains,Rat Strain, Inbred,Rat Strains, Inbred,Rat, August,Rat, Inbred Strains,Rats Inbred Strain,Rats Inbred Strains,Rats, August,Rats, Inbred Strain,Strain Rat, Inbred,Strain Rats, Inbred,Strain, Inbred Rat,Strains, Inbred Rat
D005921 Glomerulonephritis Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY. Bright Disease,Kidney Scarring,Glomerulonephritides,Scarring, Kidney

Related Publications

K Matsumoto
April 1956, The Australian journal of experimental biology and medical science,
K Matsumoto
January 1965, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society,
K Matsumoto
April 1967, Experimental and molecular pathology,
K Matsumoto
January 1963, Laboratory investigation; a journal of technical methods and pathology,
K Matsumoto
January 1964, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
K Matsumoto
October 1974, British journal of experimental pathology,
K Matsumoto
December 1990, Kidney international,
Copied contents to your clipboard!