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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kim, Soo-hyun Lewis, Eli C. Azam, Tania Reznikov, Leonid L. Lee, Jae-kwon Dinarello, Charles A. |
| Description | Author Affiliation: Lee JK ( Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.); |
| Abstract | IL-1 and IL-18 are members of the IL-1 family of ligands, and their receptors are members of the IL-1 receptor family. Although several biological properties overlap for these cytokines, differences exist. IL-18 uniquely induces IFN-gamma from T lymphocytes and natural killer cells but does not cause fever, whereas fever is a prominent characteristic of IL-1 in humans and animals. In the present study, human epithelial cells were stably transfected with the IL-18 receptor beta chain and responded to IL-18 with increased production of IL-1alpha, IL-6, and IL-8. Five minutes after exposure to either cytokine, phosphorylation of mitogen activated protein kinase (MAPK) p38 was present; specific inhibition of p38 MAPK reduced IL-18 activity to background levels. Whereas IL-1beta induced the expression of the NF-kappaB-reporter gene and was suppressed by competitive inhibition of NF-kappaB binding, IL-18 responses were weak or absent. In contrast to IL-1beta, IL-18 also did not activate degradation of the NF-kappaB inhibitor. After 4 h, both cytokines induced comparable levels of mRNA for the chemokine IL-8 but, in the same cells, steady-state levels of cyclooxygenase (COX)-2 mRNA were high after IL-1beta but low or absent after IL-18. After 30 h, IL-18-induced COX-2 appeared in part to be IL-1 dependent. Similarly, low levels of prostaglandin E2 were measured in IL-18-stimulated A549 cells and freshly obtained primary human monocytes and mouse macrophages. We conclude that in epithelial cells, IL-18 signal transduction is primarily via the MAPK p38 pathway rather than NF-kappaB, which may explain the absence of COX-2 and the failure of IL-18 to cause fever. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 23 |
| Volume Number | 101 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2004-06-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Interleukin-18 Pharmacology Interleukin-1 MAP Kinase Signaling System Drug Effects Animals Cell Line Cyclooxygenase 2 DNA, Complementary Genetics Dinoprostone Metabolism Fever Etiology In Vitro Techniques Biosynthesis Interleukin-6 Interleukin-8 Isoenzymes Macrophages Physiology Membrane Proteins Mice Mitogen-Activated Protein Kinases Monocytes NF-kappa B Phosphorylation Prostaglandin-Endoperoxide Synthases RNA, Messenger Recombinant Proteins Transcription Factor AP-1 P38 Mitogen-Activated Protein Kinases Comparative Study Research Support, U.S. Gov't, P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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