Cellular and molecular regulation of tumor necrosis factor-alpha production by pentoxofylline
Tumor necrosis factor-alpha (TNF), a mononuclear phagocyte (MO)-derived peptide, is increasingly being recognized for its pleomorphic immunologic effects. A number of investigations have demonstrated that lipopolysaccharide (LPS) can induce TNF synthesis, yet mechanisms that regulate TNF expression...
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| Published in | Biochemical and biophysical research communications Vol. 155; no. 3; pp. 1230 - 1236 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Elsevier Inc
01.09.1988
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| Online Access | Get full text |
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| Abstract | Tumor necrosis factor-alpha (TNF), a mononuclear phagocyte (MO)-derived peptide, is increasingly being recognized for its pleomorphic immunologic effects. A number of investigations have demonstrated that lipopolysaccharide (LPS) can induce TNF synthesis, yet mechanisms that regulate TNF expression at the cellular and molecular levels have not been fully elucidated. In this study, we present data demonstrating pentoxifylline, a methylxanthine, is efficacious in suppressing LPS-induced MO-derived TNF at the level of both TNF mRNA accumulation and TNF supernatant bioactivity. Pentoxifylline, at a dose of 1 × 10
−5M, suppressed the production of both biologically active TNF and TNF mRNA expression by more than 50%. Furthermore, additional methylxanthines and dibutyryl cAMP have similar effects on TNF expression. These data support the mechanism for this suppressive effect is via the generation of intracellular cAMP. |
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| AbstractList | Tumor necrosis factor-alpha (TNF), a mononuclear phagocyte (MO)-derived peptide, is increasingly being recognized for its pleomorphic immunologic effects. A number of investigations have demonstrated that lipopolysaccharide (LPS) can induce TNF synthesis, yet mechanisms that regulate TNF expression at the cellular and molecular levels have not been fully elucidated. In this study, we present data demonstrating pentoxifylline, a methylxanthine, is efficacious in suppressing LPS-induced MO-derived TNF at the level of both TNF mRNA accumulation and TNF supernatant bioactivity. Pentoxifylline, at a dose of 1 × 10
−5M, suppressed the production of both biologically active TNF and TNF mRNA expression by more than 50%. Furthermore, additional methylxanthines and dibutyryl cAMP have similar effects on TNF expression. These data support the mechanism for this suppressive effect is via the generation of intracellular cAMP. |
| Author | Strieter, R.M. Remick, D.G. Spengler, R.N. Lynch, J.P. Larrick, J. Ward, P.A. Kunkel, S.L. |
| Author_xml | – sequence: 1 givenname: R.M. surname: Strieter fullname: Strieter, R.M. organization: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Ann Arbor, Michigan, USA – sequence: 2 givenname: D.G. surname: Remick fullname: Remick, D.G. organization: Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA – sequence: 3 givenname: P.A. surname: Ward fullname: Ward, P.A. organization: Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA – sequence: 4 givenname: R.N. surname: Spengler fullname: Spengler, R.N. organization: Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA – sequence: 5 givenname: J.P. surname: Lynch fullname: Lynch, J.P. organization: Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA – sequence: 6 givenname: J. surname: Larrick fullname: Larrick, J. organization: Genelabs Inc., Redwood City, California, USA – sequence: 7 givenname: S.L. surname: Kunkel fullname: Kunkel, S.L. organization: Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA |
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