Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder

Liu, JiaJun; Buisman-Pijlman, Femke; Hutchinson, Mark R.

doi:10.3389/fnins.2014.00309

Cited by 119Tryptophan and brain disordersStress Responses and CortisolNeuroinflammation and Neurodegeneration Mechanisms

Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder

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Liu, JiaJun, Buisman-Pijlman, Femke, Hutchinson, Mark R.·2014·Frontiers in Neuroscience

DOI 10.3389/fnins.2014.00309PMC PMC4179746

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Abstract

Major depressive disorder (MDD) poses one of the highest disease burdens worldwide. Yet, current treatments targeting serotonergic and noradrenaline reuptake systems are insufficient to provide long-term relief from depressive symptoms in most patients, indicating the need for new treatment targets. Having the ability to influence behavior similar to depressive symptoms, as well as communicate with neuronal and neuroendocrine systems, the innate immune system is a strong candidate for MDD treatments. Given the complex nature of immune signaling, the main question becomes: What is the role of the innate immune system in MDD? The current review presents evidence that toll-like receptor 4 (TLR4), via driving both peripheral and central immune responses, can interact with serotonergic neurotransmission and cause neuroendocrine disturbances, thus integrating with widely observed hallmarks of MDD. Additionally, through describing the multi-directional communication between immune, neural and endocrine systems in stress, TLR4-related mechanisms can mediate stress-induced adaptations, which are necessary for the development of MDD. Therefore, apart from exogenous pathogenic mechanisms, TLR4 is involved in immune changes as a result of endogenous stress signals, playing an integral part in the pathophysiology, and could be a potential target for pharmacological treatments to improve current interventions for MDD.

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Innate immune receptors are one mechanism underlying the effect of microbiota on the HPA axis.
“Innate immune receptors are one of the mechanisms underlying the effect of microbiota on the HPA axis (Liu et al., 2014; Zacharowski et al., 2006).”
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“The immune-priming effect of stress is proposed to mediate stress-induced side effects such as allodynia (Loram et al., 2011), and drug abuse (Frank et al., 2011), and could potentially be involved in MDD as well.”
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Authors: Liu, J., Buisman-Pijlman, F., & Hutchinson, M. R.
Affiliations: The University of Adelaide (AU)
Corresponding author: Hutchinson, Mark R.
ORCID: Liu, JiaJun
Hutchinson, Mark R.
Venue: Frontiers in Neuroscience
Publisher: Frontiers Media SA
Published: 2014-09-30
Volume: 8
Pages: 309-309
ISSN: 1662-453X (ISSN-L)
DOI: 10.3389/fnins.2014.00309
PMC: PMC4179746
OpenAlex: W2033317027
Cited by: 119
References: 170
Citations by year: 2026: 9 · 2025: 5 · 2024: 9 · 2023: 14 · 2022: 10 · 2021: 13 · 2020: 12 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 13 · 2015: 7 · 2014: 3
FWCI: 3.38
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Neuroscience (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Minerva Access (University of Melbourne) (submittedVersion, cc-by)
Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: TLR4, major depressive disorder, innate immunity, neuroimmune interactions, neuroendocrine interaction, serotonergic neurotransmission, stress, neuroendocrine dysfunction, immune signaling, antidepressant targets, chronic stress

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Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder

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