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The plasma levels of various cytokines are increased during ongoing depression and are reduced to normal levels after recovery
Abstract
Background Cytokines are implicated in the pathophysiology of major depressive disorder (MDD). However, the pattern of alterations in cytokine levels is still unclear. The current study investigated the plasma levels of a range of cytokines in a follow-up design, with the aim of determining their involvement in depression.Methods Fifty medication-free MDD patients with a depressive episode and 34 healthy controls were included at baseline; the patients were followed up after 12 weeks. Before initiating treatment, the patients were diagnosed and assessed for depressive symptoms and blood for cytokine analysis was obtained. The same clinical assessments and cytokine measurements were performed after 12 weeks of "treatment as usual."Results The cytokines interleukin (IL)-1β, IL-1 receptor antagonist (IL-1Ra), IL-5, IL-6, IL-7, IL-8, IL-10, granulocyte colony-stimulating factor (G-CSF), and interferon gamma (IFNγ) were significantly elevated (p=0.01-0.047) in depressed patients at baseline compared to healthy controls. After 12 weeks of treatment, the plasma levels of seven of these nine cytokines (IL-1Ra, IL-6, IL-7, IL-8, IL-10, G-CSF, and IFNγ had decreased significantly compared to baseline and did not differ from those in the healthy controls. The depressive symptoms were simultaneously significantly reduced. In addition, the reduction to normal cytokines levels occurred only in those who met the recovery criteria.Conclusion A more general pattern of elevated cytokine levels is described herein relative to what has been described previously shown in MDD. Furthermore, recovery from depression was associated with reduction to normal levels of the majority of the measured cytokines. These results strongly support the notion that a complex network of cytokines is involved in the pathophysiology of MDD.
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“High levels of inflammation are associated with many mental health conditions including depression [29–30].”
From Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers (2016) · cites this paper as [29]
In the citing paper
“Following research showing that both acute and chronic stress and depression are associated with increases in stress hormones and inflammatory immune response [29–30]”
From Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers (2016) · cites this paper as [29]
In the citing paper
“Increased levels of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-18, tumor necrosis factor-α (TNF-α) and interferon-γ (IFNγ) have been consistently reported in the blood of depressed patients [138,139,140]”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [140]
In the citing paper
“Moreover, antidepressant treatment seem to attenuate this immunological response [140,143].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [140]
In the citing paper
“Interestingly, treatment with antidepressants can result in an antiinflammatory response throughout the brain, mitigating the inflammatory unbalance to homeostatic levels and normalizing BDNF concentrations [83, 84].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [83]
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“Keywords: Major depressive disorder Fibroblasts Inflammation Oxidative stress Mitochondrial function Lipid metabolism IL1b TNFa IL6 Cytokine”
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“, IL-1 , IL-6, IL-8, and GM-CSF) were increased in depressed patients [8].”
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“Most evidence of subgroups in depression has focused on atypical and melancholic subtypes; most frequently atypical depression has been associated with aberrant inflammation [11], but studies have also reported comparably elevated inflammation in melancholic and atypical [13] or non-melancholic depression [14].”
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“There is also some evidence showing that recovery from depressive disorder correlates with return of the inflammatory state to normality [4].”
BackgroundMicrobiome‐skin‐brain axis: A novel paradigm for cutaneous wounds
Hadian, Y., Fregoso, D. R., Nguyen, C., Bagood, M. D., Dahle, S. E., Gareau, M. G., & Isseroff, R. R. (2020) · Wound Repair and Regeneration · doi:10.1111/wrr.12800 · Cited by 26
Waheed, A., Dalton, B., Wesemann, U., Ibrahim, M. A. A., & Himmerich, H. (2018) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2017.0088 · Cited by 23
Chronic inflammation as a potential mediator between phthalate exposure and depressive symptoms
Bao, C., Lv, J., Chen, J., Wei, G.-Z., Liu, N., Wang, Y., Ding, Z., Liu, W., Li, X., Cao, H., et al. (2022) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2022.113313 · Cited by 23
Wang, Q., Zeng, L., Hong, W., Luo, M., Zhao, N., Hu, X., Shi, M., Qiu, J., Shen, Y., Teng, X., et al. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.925007 · Cited by 22
“(40) found that, compared with HC, the IFN-γ level of untreated patients with depression was significantly higher.”
ResultZhao, T., Piao, L.-H., Li, D.-P., Xu, S., Wang, S., Yuan, H., & Zhang, C. (2022) · Journal of Affective Disorders · doi:10.1016/j.jad.2022.12.035 · Cited by 22
Kim, H., Baek, S.-H., Kim, J., Ryu, S., Lee, J., Kim, J., Chung, Y., & Kim, S. (2023) · Schizophrenia · doi:10.1038/s41537-023-00398-1 · Cited by 26
“Moreover, several studies have found changes in in fl ammatory cytokine levels in patients with schizophrenia 7,8 .”
BackgroundYang, K., Liu, M., Liou, Y., Hu, L., Yang, B., & Chou, Y.-H. (2021) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2021.01.018 · Cited by 22
Reduced MIP-1β as a Trait Marker and Reduced IL-7 and IL-12 as State Markers of Anorexia Nervosa
Keeler, J. L., Patsalos, O., Chung, R., Schmidt, U. H., Breen, G. D., Treasure, J. L., Himmerich, H., & Dalton, B. (2021) · Journal of Personalized Medicine · doi:10.3390/jpm11080814 · Cited by 22
Bai, H., Chen, S., Yuan, T., Xu, D., Cui, S.-B., & Li, X. (2021) · Korean Journal of Physiology and Pharmacology · doi:10.4196/kjpp.2021.25.3.217 · Cited by 21
“Once stimulated, IB kinase participates in the phosphorylation and ubiquitin-mediated degradation of NF-B through the proteasome pathway, so that NF-B can be released and enter the nucleus to perform transcriptional activation, thereby activating the release of various inflammatory factors [40,41].”
BackgroundChen, S., Zhang, Y., & Yuan, Y. (2021) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s322078 · Cited by 21
Ormstad, H., Dahl, J., Verkerk, R. M., Andreassen, O. A., & Maes, M. H. J. (2016) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2016.05.005 · Cited by 21
“We have recently reported a broader activation of the cytokine network in MDD (Dahl et al., 2014).”
InfluentialSelf-citationMilenkovic, V. M., Sarubin, N., Hilbert, S., Baghai, T. C., Stöffler, F., Lima‐Ojeda, J. M., Manook, A., Almeqbaali, K., Wetzel, C. H., Rupprecht, R., et al. (2017) · NeuroImmunoModulation · doi:10.1159/000479739 · Cited by 21
Xia, J., Lu, Z., Feng, S., Yang, J., & Ji, M. (2018) · International Immunopharmacology · doi:10.1016/j.intimp.2018.03.010 · Cited by 22
Rachayon, M., Jirakran, K., Sodsai, P., Klinchanhom, S., Sughondhabirom, A., Plaimas, K., Suratanee, A., & Maes, M. H. J. (2022) · Pharmaceuticals · doi:10.3390/ph15040405 · Cited by 21
“Other authors found increased IL-5 levels in medication-free MDD patients and MDD patients with or without obesity as comorbidity [50,51].”
BackgroundTagliarini, C., Carbone, M. G., Pagni, G., Marazziti, D., & Pomara, N. (2020) · CNS Spectrums · doi:10.1017/s1092852920001959 · Cited by 21
The NLRP3 Inflammasome in Stress Response: Another Target for the Promiscuous Cannabidiol
dos Santos, A. H., Vila-Verde, C., Guimarães, F. S., Joca, S. R. L., & Lisboa, S. F. D. S. (2022) · Current Neuropharmacology · doi:10.2174/1570159x20666220411101217 · Cited by 20
“br From another perspective, several studies report increased inflammation markers, for example, in many cases evaluated in untreated affective disorder patients [2, 10], or PTSD patients [11].”
How to assess stress biomarkers for idiographic research?
van Ockenburg, S. L., Booij, S. H., Riese, H., Rosmalen, J. G. M., & Janssens, K. A. M. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2015.08.002 · Cited by 21
“Immune biomarkers do not only show large fl uctuations over time (Haberkorn et al., 2013; Schubert et al., 2012), but have also shown to be good predictors of physical and sometimes even mental illness (e.g., Dahl et al., 2014).”
Wu, X., Chen, Z., Liao, Y., Yang, Z., Liang, X., Guan, N., & Gan, Z. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.1063479 · Cited by 23
“In recent years, antiinflammatory agents were expected to be a promising treatment target of MDD (39) and BDD (40).”
ResultInfluentialRömer, J., Klein, A., & Horneff, G. (2023) · Rheumatology International · doi:10.1007/s00296-023-05323-4 · Cited by 19
Bauer, O., Milenkovic, V. M., Hilbert, S., Sarubin, N., Weigl, J., Bahr, L., Wetter, T. C., Heckel, B., Wetzel, C. H., Rupprecht, R., et al. (2020) · NeuroImmunoModulation · doi:10.1159/000513093 · Cited by 19
Sun, T., Peng, R., Sun, X., & Li, Y. (2021) · Brain Sciences · doi:10.3390/brainsci11121612 · Cited by 18
“Findings on depression in patients who displayed increased levels of peripheral inflammatory factors such as IL-6 [17,18], CRP [19], and TNF-α [20] can confirm this.”
BackgroundAndreou, B., Reid, B. E., Lyall, A. E., Karayumak, S. C., Kubicki, A., Espinoza, R. T., Kruse, J. L., Narr, K. L., & Kubicki, M. R. (2022) · Translational Psychiatry · doi:10.1038/s41398-022-01960-8 · Cited by 18
“Research has suggested that MDD is due, in part, to a dysfunction of the immune response, with MDD patients exhibiting higher levels of circulating pro-inflammatory cytokines in the peripheral blood compared to healthy individuals [3, 6].”
BackgroundChen, B. K., & Denny, C. A. (2022) · Neuropharmacology · doi:10.1016/j.neuropharm.2022.109345 · Cited by 19
Akter, M. S., Emon, F. A., Nahar, Z., Qusar, M. S., Islam, S. M. A., Shahriar, M., Bhuiyan, M. A., & Islam, M. R. (2023) · BMC Psychiatry · doi:10.1186/s12888-023-05354-y · Cited by 19
“Therefore, it is crucial to identify and define biological risk factors to understand the etiology and treatment of depression [72].”
BackgroundManagement of Infant Atopic Eczema to Prevent Severe Eczema and Food Allergy
Yamamoto‐Hanada, K., & Ohya, Y. (2024) · Clinical & Experimental Allergy · doi:10.1111/cea.14515 · Cited by 20
“Depression [50, 51], for instance, induces changes in cytokine levels in the blood [52], impacting immune function.”
Biomarker-Guided Tailored Therapy
Lydiard, J. B., & Nemeroff, C. B. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-32-9721-0_10 · Cited by 20
Yamasaki, K., Hasegawa, T., & Takeda, M. (2020) · Neuropsychopharmacology Reports · doi:10.1002/npr2.12100 · Cited by 19
Bocharova, M., Borza, T., Watne, L. O., Engedal, K., O'Brien, J. T., Selbæk, G., Idland, A., Hodsoll, J. P., Young, A. H., & Aarsland, D. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-02908-2 · Cited by 19
Gędek, A., Modrzejewski, S., Materna, M., Iwański, M., Wichniak, A., & Dominiak, M. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262110362 · Cited by 18
In Silico Study Examining New Phenylpropanoids Targets with Antidepressant Activity
Calixto, P. D. S., de Almeida, R. N., Salvadori, M. G. D. S. S., Maia, M. D. S., Barbosa‐Filho, J. M., Scotti, L., & Scotti, L. (2020) · Current Drug Targets · doi:10.2174/1389450121666200902171838 · Cited by 18
Desfossés, C.-Y., Peredo, R., Chabot, A., Carmel, J.-P., Tremblay, P.-M., Mérette, C., Picher, G., Lachance, I., Patry, S., & Lemasson, M. (2021) · Journal of Ect · doi:10.1097/yct.0000000000000782 · Cited by 17
Cheng, Y., Zhu, Z., Yang, Z., Liu, X., Qian, X., Zhu, J., Hu, X., Jiang, P., Cui, T., Wang, Y., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-97369-6 · Cited by 21
“Notably, TNF-α, a key inflammatory mediator, is consistently elevated in depressed individuals and associated with various neuropsychiatric disorders 12,13,97 .”
Metadata
- Authors
- Dahl, J., Ormstad, H., Aass, H. C. D., Malt, U. F., Bendz, L. T., Sandvik, L., Brundin, L., & Andreassen, O. A.
- Affiliations
- Vestre Viken Hospital Trust (NO)
- Buskerud University College (NO)
- Oslo University Hospital (NO)
- Van Andel Institute (US)
- Corresponding author
- Dahl, Johan
- ORCID
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 45
- Pages
- 77-86
- ISSN
- 0306-4530 (ISSN-L)
- OpenAlex
- W2134586420
- Cited by
- 424
- References
- 53
- Citations by year
- 2026: 15 · 2025: 22 · 2024: 30 · 2023: 75 · 2022: 35 · 2021: 50 · 2020: 36 · 2019: 37 · 2018: 30 · 2017: 34 · 2016: 33 · 2015: 19 · 2014: 7
- FWCI
- 9.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Helse Sør-Øst RHF
- 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, cytokines, plasma cytokines, interleukin-6, IL-10, interleukin-1 receptor antagonist, interferon-gamma, granulocyte colony-stimulating factor, recovery from depression, usual care
- MeSH terms
- Adult, Antidepressive Agents, Major Depressive Disorder, Female, Humans, Male, Middle Aged, Severity of Illness Index, Up-Regulation, Case-Control Studies, Cytokines, Treatment Outcome, Inflammation Mediators, Recovery of Function
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