Macrophage membrane interleukin 1 regulates the expression of acute phase proteins in human hepatoma Hep 3B cells

• Published in: The Journal of immunology (1950) Vol. 139; no. 6; pp. 1896 - 1901
• Main Authors: Beuscher, HU, Fallon, RJ, Colten, HR
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-09-1987; American Association of Immunologists
• Subjects: Acute-Phase Proteins - biosynthesis; Albumins - biosynthesis; Analysis of the immune response. Humoral and cellular immunity; Biological and medical sciences; Carcinoma, Hepatocellular; Cell Line; Cell Membrane - physiology; Complement C3 - biosynthesis; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Gene Expression Regulation; Humans; Immunobiology; Interleukin-1 - physiology; Lipopolysaccharides - pharmacology; Liver - metabolism; Liver Neoplasms; Lymphokines, interleukins ( function, expression); Macrophages - physiology; Molecular Weight; Regulatory factors and their cellular receptors; RNA, Messenger - genetics; Human; Membrane protein; Complement C3; Albumin; Interleukin 1α; Monokine; Biosynthesis; Gene expression; Immunochemistry; Acute phase protein; Regulation(control); Antiserum; Cell line; Liver cell carcinoma; Interleukin 1; Macrophage
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.139.6.1896

To assess the potential role of membrane interleukin 1 (mIL-1) in modulating expression of acute phase proteins, we studied the effect of fixed mouse peritoneal macrophages and isolated cell membranes on the synthesis of C3 and albumin in human hepatoma Hep 3B cells. An increase in C3 synthesis and decrease in albumin synthesis were detected after incubation of Hep 3B cells with fixed stimulated macrophages or with membrane preparations. Estimates of hepatocellular C3 and albumin mRNA indicated that the mIL-1 regulation was exerted at a pretranslational level. The changes in C3 and albumin expression induced by mIL-1 were inhibited by addition of anti-interleukin 1 (IL-1) antiserum to the macrophages, supporting the hypothesis that a form of IL-1 is present on the outer cell membrane of macrophages. Moreover, cell-surface iodination of macrophages allowed the detection of a 33-kDa IL-1 molecule, suggesting that an IL-1 species, similar to the intracellular precursor of IL-1 is present at the outer cell surface of macrophages. The expression of mIL-1 was temporally dissociated from IL-1 release, indicating that the cell-surface associated IL-1 activity is not the result of adsorbed soluble IL-1. These studies provide a basis for further investigation of the role of mIL-1 in modulating monocytes and macrophages function via cell-cell interactions.