ArticleBrain, behavior, and immunity2015
Peripheral indoleamine 2,3-dioxygenase 1 is required for comorbid depression-like behavior but does not contribute to neuropathic pain in mice.
Article in Brain, behavior, and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- The Role of Bacteria and Its Derived Metabolites in Chronic Pain and Depression: Recent Findings and Research Progress.The international journal of neuropsychopharmacology · 2020Pooled it
- The role of the kynurenine pathway in the pathogenesis of pain and affective disorders after traumatic brain injury.Brain, behavior, & immunity - health · 2026Review
- Indoleamine 2,3-Dioxygenase: A Potential Biomarker for Neural Damage Severity of Leprosy Neuropathy.Cellular and molecular neurobiology · 2026Article
- The Role of Gut-Brain Tryptophan Metabolism and Fatty Acid Peroxidation in the Effect of Sleep Deprivation on Anxiety and Depression in PCOS Mice.Molecular neurobiology · 2025Article
- Indoleamine-2,3-dioxygenase: An important controller in maintaining mesenchymal stem cell-mediated immunomodulatory homeostasis.Acta pharmaceutica Sinica. B · 2025Review
- Ghrelin/GHSR System in Depressive Disorder: Pathologic Roles and Therapeutic Implications.Current issues in molecular biology · 2024Review
- Targeting Underlying Inflammation in Carcinoma Is Essential for the Resolution of Depressiveness.Cells · 2023Review
- Meningeal dendritic cells drive neuropathic pain through elevation of the kynurenine metabolic pathway in mice.The Journal of clinical investigation · 2022Article
- The Role of Kynurenine and Its Metabolites in Comorbid Chronic Pain and Depression.Metabolites · 2022Review
- The Kynurenine Pathway as a Potential Target for Neuropathic Pain Therapy Design: From Basic Research to Clinical Perspectives.International journal of molecular sciences · 2021Review
- Preclinical Considerations about Affective Disorders and Pain: A Broadly Intertwined, yet Often Under-Explored, Relationship Having Major Clinical Implications.Medicina (Kaunas, Lithuania) · 2020Review
- The Role of the Kynurenine Signaling Pathway in Different Chronic Pain Conditions and Potential Use of Therapeutic Agents.International journal of molecular sciences · 2020Review
- Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain.International journal of molecular sciences · 2020Review
- Neuroinflammation, Pain and Depression: An Overview of the Main Findings.Frontiers in psychology · 2020Review
- Kynurenine, Tetrahydrobiopterin, and Cytokine Inflammatory Biomarkers in Individuals Affected by Diabetic Neuropathic Pain.Frontiers in neuroscience · 2020Article
- Resolution of inflammation-induced depression requires T lymphocytes and endogenous brain interleukin-10 signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Effects of anti-inflammatory drugs on the expression of tryptophan-metabolism genes by human macrophages.Journal of leukocyte biology · 2018Article
- p38 predicts depression and poor outcome in esophageal cancer.Oncology letters · 2017Article
- Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain.Brain, behavior, and immunity · 2017Article
- Pifithrin-μ Prevents Cisplatin-Induced Chemobrain by Preserving Neuronal Mitochondrial Function.Cancer research · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic pain frequently co-occurs with major depressive disorder but the mechanisms are poorly understood. We investigated the contribution of indoleamine 2,3-dioxygenase-1 (IDO1), a rate-limiting enzyme in the conversion of tryptophan to neurotoxic metabolites, to this comorbidity using the spared nerve injury (SNI) model of neuropathic pain in mice. SNI resulted in unilateral mechanical allodynia, reduced social interaction, and increased immobility in the forced swim test without changes in locomotor activity. These findings indicate SNI-induced pain and comorbid depression-like behavior. These behavioral responses were accompanied by increases in plasma kynurenine/tryptophan ratios and increased expression of Ido1 and Il1b mRNA in the liver. Interestingly, SNI did not induce detectable changes in spinal cord or brain Ido1 mRNA levels. SNI was associated with spinal cord inflammatory activity as evidenced by increased Il1b mRNA expression. The SNI-induced increase of liver Ido1and Il1b mRNA was abrogated by intrathecal administration of the IL-1 inhibitor IL-1RA. Intrathecal IL-1RA also inhibited both mechanical allodynia and depression-like behavior. We also show that Ido1 is required for the development of depression-like behavior because Ido1(-/-) mice do not develop increased immobility in the forced swim test or decreased social exploration in response to SNI. Mechanical allodynia was similar in WT and Ido1(-/-) mice. In conclusion, our findings show for the first time that neuropathic pain is associated with an increase of Ido1 in liver, but not brain, downstream of spinal cord IL-1β signaling and that Ido1 mediates comorbid depression. Moreover, comorbidity of neuropathic pain and depression are only partially mediated by a common mechanism because mechanical hyperalgesia develops independently of Ido1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.