Cutting Edge: Stat6-Dependent Substrate Depletion Regulates Nitric Oxide Production
The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4 and IL-13 regulate NO production through depletion of arginine, the substrate of inducible NO synthase (iNOS). Inhibition of NO production from murin...
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| Published in | The Journal of immunology (1950) Vol. 166; no. 4; pp. 2173 - 2177 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Am Assoc Immnol
15.02.2001
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4 and IL-13 regulate NO production through depletion of arginine, the substrate of inducible NO synthase (iNOS). Inhibition of NO production from murine macrophages stimulated with LPS and IFN-gamma by IL-4 or IL-13 was dependent on Stat6, cell density in the cultures, and pretreatment for at least 6 h. IL-4/IL-13 did not interfere with the expression or activity of iNOS but up-regulated arginase I (the liver isoform of arginase) in a Stat6-dependent manner. Addition of exogenous arginine completely restored NO production in IL-4-treated macrophages. Furthermore, impaired killing of the intracellular pathogen Toxoplasma gondii in IL-4-treated macrophages was overcome by supplementing L-arginine. The simple system of regulated substrate competition between arginase and iNOS has implications for understanding the physiological regulation of NO production. |
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| AbstractList | The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4 and IL-13 regulate NO production through depletion of arginine, the substrate of inducible NO synthase (iNOS). Inhibition of NO production from murine macrophages stimulated with LPS and IFN-gamma by IL-4 or IL-13 was dependent on Stat6, cell density in the cultures, and pretreatment for at least 6 h. IL-4/IL-13 did not interfere with the expression or activity of iNOS but up-regulated arginase I (the liver isoform of arginase) in a Stat6-dependent manner. Addition of exogenous arginine completely restored NO production in IL-4-treated macrophages. Furthermore, impaired killing of the intracellular pathogen Toxoplasma gondii in IL-4-treated macrophages was overcome by supplementing L-arginine. The simple system of regulated substrate competition between arginase and iNOS has implications for understanding the physiological regulation of NO production. Abstract The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4 and IL-13 regulate NO production through depletion of arginine, the substrate of inducible NO synthase (iNOS). Inhibition of NO production from murine macrophages stimulated with LPS and IFN-γ by IL-4 or IL-13 was dependent on Stat6, cell density in the cultures, and pretreatment for at least 6 h. IL-4/IL-13 did not interfere with the expression or activity of iNOS but up-regulated arginase I (the liver isoform of arginase) in a Stat6-dependent manner. Addition of exogenous arginine completely restored NO production in IL-4-treated macrophages. Furthermore, impaired killing of the intracellular pathogen Toxoplasma gondii in IL-4-treated macrophages was overcome by supplementing l-arginine. The simple system of regulated substrate competition between arginase and iNOS has implications for understanding the physiological regulation of NO production. |
| Author | Lang, Roland Wynn, Thomas A Ihle, James N Hesse, Matthias Murray, Peter J Rutschman, Robert |
| Author_xml | – sequence: 1 fullname: Rutschman, Robert – sequence: 2 fullname: Lang, Roland – sequence: 3 fullname: Hesse, Matthias – sequence: 4 fullname: Ihle, James N – sequence: 5 fullname: Wynn, Thomas A – sequence: 6 fullname: Murray, Peter J |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11160269$$D View this record in MEDLINE/PubMed |
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| Snippet | The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4 and... Abstract The cytokines IL-4 and IL-13 inhibit the production of NO from activated macrophages through an unresolved molecular mechanism. We show here that IL-4... |
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| SubjectTerms | Animals Arginase - biosynthesis Arginine - deficiency Cells, Cultured Down-Regulation - immunology Interleukin-13 - physiology Interleukin-4 - physiology Macrophage Activation Macrophages, Peritoneal - enzymology Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - parasitology Mice Mice, Inbred C57BL Mice, Knockout Nitric Oxide - antagonists & inhibitors Nitric Oxide - biosynthesis Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II STAT6 Transcription Factor Substrate Specificity - immunology Toxoplasmosis, Animal - enzymology Toxoplasmosis, Animal - immunology Toxoplasmosis, Animal - metabolism Trans-Activators - deficiency Trans-Activators - genetics Trans-Activators - physiology |
| Title | Cutting Edge: Stat6-Dependent Substrate Depletion Regulates Nitric Oxide Production |
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