Cited by 212Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsTreatment of Major Depression

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Antidepressant therapies inhibit inflammation and microglial M1-polarization

Kalkman, Hans O., Feuerbach, Dominik·2016·Pharmacology & Therapeutics

DOI 10.1016/j.pharmthera.2016.04.001

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Abstract

Macrophages and their counterparts in the central nervous system, the microglia, detect and subsequently clear microbial pathogens and injured tissue. These phagocytic cells alter and adapt their phenotype depending on their prime activity, i.e., whether they participate in acute defence against pathogenic organisms ('M1'-phenotype) or in clearing damaged tissues and performing repair activities ('M2'-phenotype). Stimulation of pattern recognition receptors by viruses (vaccines), bacterial membrane components (e.g., LPS), alcohol, or long-chain saturated fatty acids promotes M1-polarization. Vaccine or LPS administration to healthy human subjects can result in sickness symptoms and low mood. Alcohol abuse and abdominal obesity are recognized as risk factors for depression. In the M1-polarized form, microglia and macrophages generate reactive oxygen and nitrogen radicals to eradicate microbial pathogens. Inadvertently, also tetrahydrobiopterin (BH4) may become oxidized. This is an irreversible reaction that generates neopterin, a recognized biomarker for depression. BH4 is a critical cofactor for the synthesis of dopamine, noradrenaline, and serotonin, and its loss could explain some of the symptoms of depression. Based on these aspects, the suppression of M1-polarization would limit the inadvertent catabolism of BH4. In the current review, we evaluate the evidence that antidepressant treatments (monoamine reuptake inhibitors, PDE4 inhibitors, lithium, valproate, agomelatine, tianeptine, electroconvulsive shock, and vagus nerve stimulation) inhibit LPS-induced microglia/macrophage M1-polarization. Consequently, we propose that supplementation with BH4 could limit the reduction in central monoamine synthesis and might represent an effective treatment for depressed mood.

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Authors: Kalkman, H. O., & Feuerbach, D.
Affiliations: Novartis Institutes for BioMedical Research (CH)
Corresponding author: Kalkman, Hans O.
Venue: Pharmacology & Therapeutics
Publisher: Elsevier BV
Published: 2016-07
Volume: 163
Pages: 82-93
ISSN: 0163-7258 (ISSN-L)
DOI: 10.1016/j.pharmthera.2016.04.001
OpenAlex: W2339641321
Semantic Scholar: af6eac8dc2429b5d773109dd9d983af827f3749c
Cited by: 212
References: 204
Citations by year: 2026: 7 · 2025: 31 · 2024: 20 · 2023: 35 · 2022: 31 · 2021: 31 · 2020: 20 · 2019: 16 · 2018: 7 · 2017: 14
FWCI: 0.75
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Pharmacology & Therapeutics (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Keywords: antidepressants, microglial M1 polarization, neuroinflammation, tetrahydrobiopterin, neopterin, lipopolysaccharide, macrophages, depression, monoamine synthesis, BH4 supplementation, phosphodiesterase-4 inhibitors, lithium, valproic acid, agomelatine, tianeptine, electroconvulsive therapy, vagus nerve stimulation, monoamine reuptake inhibitors
MeSH terms: Animals, Antidepressive Agents, Biopterins, Depression, Electroconvulsive Therapy, Humans, Inflammation, Lipopolysaccharides, Macrophages, Phenotype, Risk Factors, Stress, Psychological, Signal Transduction, Biomarkers, Microglia

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Antidepressant therapies inhibit inflammation and microglial M1-polarization

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