Inflammation-associated depression: From serotonin to kynurenine
In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for...
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| Published in | Psychoneuroendocrinology Vol. 36; no. 3; pp. 426 - 436 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.04.2011
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0306-4530 1873-3360 1873-3360 |
| DOI | 10.1016/j.psyneuen.2010.09.012 |
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| Abstract | In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptotphan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. |
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| AbstractList | Summary In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptotphan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptotphan degrading enzyme indoleamine 2,3 dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms.In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. |
| Author | Lawson, Marcus A. Dantzer, Robert Kelley, Keith W. O’Connor, Jason C. |
| AuthorAffiliation | 2 Department of Pharmacology, The University of Texas Health Science Center at San Antonio, 216B Medical Building, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900 1 Integrative Immunology and Behavior Program, Department of Animal Sciences and Department of Medical Pathology, 227 ERML, 1201 W Gregory Drive, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801 |
| AuthorAffiliation_xml | – name: 1 Integrative Immunology and Behavior Program, Department of Animal Sciences and Department of Medical Pathology, 227 ERML, 1201 W Gregory Drive, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801 – name: 2 Department of Pharmacology, The University of Texas Health Science Center at San Antonio, 216B Medical Building, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900 |
| Author_xml | – sequence: 1 givenname: Robert surname: Dantzer fullname: Dantzer, Robert email: dantzer@illinois.edu, rosemarie.bluthe31@orange.fr organization: Integrative Immunology and Behavior Program, Department of Animal Sciences and Department of Medical Pathology, 227 Edward R. Madigan Laboratory, 1201 West Gregory Drive, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA – sequence: 2 givenname: Jason C. surname: O’Connor fullname: O’Connor, Jason C. organization: Department of Pharmacology, The University of Texas Health Science Center at San Antonio, 216B Medical Building, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA – sequence: 3 givenname: Marcus A. surname: Lawson fullname: Lawson, Marcus A. organization: Integrative Immunology and Behavior Program, Department of Animal Sciences and Department of Medical Pathology, 227 Edward R. Madigan Laboratory, 1201 West Gregory Drive, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA – sequence: 4 givenname: Keith W. surname: Kelley fullname: Kelley, Keith W. organization: Integrative Immunology and Behavior Program, Department of Animal Sciences and Department of Medical Pathology, 227 Edward R. Madigan Laboratory, 1201 West Gregory Drive, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21041030$$D View this record in MEDLINE/PubMed |
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| Snippet | In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an... Summary In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic... |
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| SubjectTerms | Animals Cytokines - metabolism Cytokines - physiology Depression Depression - etiology Disease Models, Animal Endocrinology & Metabolism Humans Indoleamine 2,3-dioxygenase Inflammation Inflammation - complications Interferon-alpha Kynurenic acid Kynurenine Kynurenine - metabolism Kynurenine - physiology Models, Biological Psychiatry Quinolinic acid Serotonin - metabolism Serotonin - physiology Signal Transduction - physiology Tryptophane |
| Title | Inflammation-associated depression: From serotonin to kynurenine |
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