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Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression
Open accessAbstract
Recognition that inflammation may represent a common mechanism of disease has been extended to include neuropsychiatric disorders including major depression. Patients with major depression have been found to exhibit increased peripheral blood inflammatory biomarkers, including inflammatory cytokines, which have been shown to access the brain and interact with virtually every pathophysiologic domain known to be involved in depression, including neurotransmitter metabolism, neuroendocrine function, and neural plasticity. Indeed, activation of inflammatory pathways within the brain is believed to contribute to a confluence of decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of glial elements, consistent with neuropathologic findings that characterize depressive disorders. Further instantiating the link between inflammation and depression are data demonstrating that psychosocial stress, a well-known precipitant of mood disorders, is capable of stimulating inflammatory signaling molecules, including nuclear factor kappa B, in part, through activation of sympathetic nervous system outflow pathways. Interestingly, depressed patients with increased inflammatory biomarkers have been found to be more likely to exhibit treatment resistance, and in several studies, antidepressant therapy has been associated with decreased inflammatory responses. Finally, preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication. Translational implications of these findings include the unique opportunity to identify relevant patient populations, apply immune-targeted therapies, and monitor therapeutic efficacy at the level of the immune system in addition to behavior.
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In the citing paper
“Patients with major depressive disorder exhibit all of the cardinal features of an inflammatory response, including increased expression of pro-inflammatory cytokines and their receptors and increased levels of acute-phase reactants, chemokines and soluble adhesion molecules in peripheral blood and cerebrospinal fluid (CSF)16,17.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [16]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, prolonged inflammatory signaling, such as when the inflammatory response is maintained by ongoing psychosocial stress, can have detrimental effects that include risk for depression and other psychiatric diseases (Dantzer et al., 2008; Miller et al., 2009; Miller and Raison, 2016; Slavich and Irwin, 2014).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Miller et al., 2009
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we found, like others,14 that SSRI might have a beneficial effect on inflammation”
From Association of depressive disorders, depression characteristics and antidepressant medication with inflammation (2012) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Earlier studies found decreases in inflammatory marker levels after antidepressant treatment, mainly SSRI (see ref. 14 for an overview)”
From Association of depressive disorders, depression characteristics and antidepressant medication with inflammation (2012) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Meta-analyses of the literature conclude that peripheral blood IL-1β, IL-6, TNF and C-reactive protein (CRP) are the most reliable biomarkers of inflammation in patients with depression16.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [16]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“increased expression of a variety of innate immune genes and proteins, including IL-1β, IL-6, TNF, Toll-like receptor 3 (TLR3) and TLR4, has been found in post-mortem brain samples from suicide victims that had depression16,18,19,21.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [16]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“is sufficient to induce depressive-like behavior in rodent models”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“is activated in conditions associated with depression in humans and in rodent models”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“As a consequence of these lingering effects, childhood adversity may predispose individuals to complicated depressions, characterized by treatment non-response, residual mood symptoms, or frequent relapse (3, 35).”
From Clustering of depression and inflammation in adolescents previously exposed to childhood adversity (2012) · cites this paper as [3]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“the inflammatory cytokine interleukin-6 (IL-6) is elevated in the serum of a subset of depressed patients”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“a growing recognition that immune system actions profoundly impact mood regulation (3–6)”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“The growing evidence of causative links between inflammation and depression (3, 4) indicates that targets of inflammatory molecules contribute to establishing a pro-depressant environment.”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“Most center around the notion that stress triggers the release of pro-inflammatory cytokines, which access the central nervous system, eliciting neurobehavioral adjustments that manifest as depressive symptoms (3–5).”
From Clustering of depression and inflammation in adolescents previously exposed to childhood adversity (2012) · cites this paper as [3]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“whereas deletion of the IL-6 gene is protective (3–5, 8)”
From Inflammatory T helper 17 cells promote depression-like behavior in mice (2013) · cites this paper as [4]
Experimental — accuracy not yet measuredIn the citing paper
“Experimental data indicate that acute psychosocial stress (e.g., public speaking, mental arithmetic) stimulates inflammatory signaling molecules194, and these responses are exaggerated in patients with depression190.”
From Psychobiological factors of resilience and depression in late life (2019) · cites this paper as [190]
In the citing paper
“Both younger190 and older191 adults with depression show increased levels of inflammatory cytokines, secreted proteins that interact with virtually every depression-relevant neurophysiological domain (e.g., neurotransmitter metabolism, neuroendocrine function, and neural plasticity).”
From Psychobiological factors of resilience and depression in late life (2019) · cites this paper as [190]
In the citing paper
“A wealth of evidence has implicated inflammation in the development of depression.”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Miller et al., 2009
In the citing paper
“Cytokines also have the capability of influencing neurocircuitry and neurotransmitter systems to produce behavioral alterations (Miller et al., 2009, Haroon et al., 2012).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Miller et al., 2009
In the citing paper
“Furthermore, administration of cytokines to humans and laboratory animals produces neuropsychiatric symptoms and behavioral alterations consistent with depression (Miller et al., 2009).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Miller et al., 2009
In the citing paper
“Interestingly, all of these pathways have been demonstrated to be affected by inflammatory cytokines (Pace et al., 2007, Dantzer et al., 2008, Miller et al., 2009, Haroon et al., 2012) (Figure 1).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Miller et al., 2009
In the citing paper
“In addition, IL-6 and IL-1β may contribute to the pathophysiology of a subset of patients with MDD via excessive release of corticotrophin releasing hormone (CRH) and by the promotion glucocorticoid receptor resistance, which may ultimately impair the negative feedback regulation of the HPA axis (59,60).”
From Peripheral cytokine and chemokine alterations in depression: a meta‐analysis of 82 studies (2017) · cites this paper as [59]
In the citing paper
“central nervous system (CNS) inflammation has been suggested to play a significant role in MDD pathogenesis due to findings of increased proinflammatory cytokines levels in patients with neurodegeneration and symptoms of depression such as anhedonia, depressed mood, and lethargy (Miller et al., 2009).”
From A Review of the Relationship between Proinflammatory Cytokines and Major Depressive Disorder (2014) · cites this paper as Miller et al., 2009
In the citing paper
“depressed patients with increased inflammatory biomarkers are more likely to be resistant to antidepressant therapy, a response to treatment has been associated with decreased inflammatory responses”
From Glucocorticoids, cytokines and brain abnormalities in depression (2011) · cites this paper as Miller et al., 2009
In the citing paper
“however, increasing preclinical and clinical evidence suggests that higher levels of oxidative stress, alterations in the Keap1-Nrf2 pathway, and Nrf2-associated inflammation are involved in the pathogenesis of these psychiatric disorders [128,129,130,131,132].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [129]
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Metadata
- Authors
- Miller, A. H., Maletic, V., & Raison, C. L.
- Affiliations
- Emory University (US)
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2009-05
- Volume
- 65
- Issue
- 9
- Pages
- 732-741
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2680424
- OpenAlex
- W1996454121
- Cited by
- 3,848
- References
- 121
- Citations by year
- 2026: 163 · 2025: 243 · 2024: 237 · 2023: 226 · 2022: 263 · 2021: 318 · 2020: 277 · 2019: 229 · 2018: 263 · 2017: 216 · 2016: 244 · 2015: 255 · 2014: 220 · 2013: 206 · 2012: 180
- FWCI
- 6.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000454)
- National Heart, Lung, and Blood Institute (R01HL073921)
- National Institute of Mental Health (R01MH083746, K23MH064619, T32MH020018, R01MH070553, K05MH069124)
- National Center for Research Resources (M01-RR00039, M01RR000039)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- major depressive disorder, inflammation, cytokines, inflammatory markers, neuroinflammation, neurotrophic support, glutamate release, oxidative stress, excitotoxicity, neuroendocrine function, neuroplasticity, psychosocial stress, NF-κB, sympathetic nervous system, antidepressant resistance, immune-targeted therapy, treatment response
- MeSH terms
- Animals, Anti-Inflammatory Agents, Basal Ganglia, Brain, Major Depressive Disorder, Depressive Disorder, Major, Humans, Inflammation, Neuronal Plasticity, Neurosecretory Systems, Stress, Psychological, Biomarkers, Cytokines, Neurotransmitter Agents
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