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Article

Inflammatory versus Anti-Inflammatory Profiles in Major Depressive Disorders—The Role of IL-17, IL-21, IL-23, IL-35 and Foxp3

1
Department of Psychotherapy, Medical University of Lodz, 91-229 Lodz, Poland
2
Department of Adult Psychiatry, Medical University of Lodz, 91-229 Lodz, Poland
3
Department of Medical Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland
4
Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
5
IMPACT—The Institute for Mental and Physical Health and Clinical Translation, School of Medicine, Barwon Health, Deakin University, Geelong, VIC 3220, Australia
6
Orygen, The National Centre of Excellence in Youth Mental Health, 35 Poplar Road, Parkville, VIC 3052, Australia
7
The Department of Psychiatry and The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3010, Australia
8
An-Nan Hospital, China Medical University, Tainan 709, Taiwan
*
Author to whom correspondence should be addressed.
J. Pers. Med. 2021, 11(2), 66; https://doi.org/10.3390/jpm11020066
Received: 11 December 2020 / Revised: 18 January 2021 / Accepted: 20 January 2021 / Published: 23 January 2021
Background: The authors of this research study intended to verify whether there are any changes in gene expression in depressed patients without coexisting inflammatory diseases for selected immune-inflammatory factors that are particularly important in autoimmune disease pathogenesis (IL-17, IL-21, IL-23, IL-35, Foxp3). Methods: The study was carried out on a group of 190 patients with depression and 100 healthy volunteers. The severity of depressive symptoms was assessed using the Hamilton Depression Scale. RT-PCR was used to evaluate mRNA expression and ELISA was used to measure protein expression of these genes. Results: The level of gene expression for IL-17, IL-21, IL-23, and IL-35 was substantially higher in the group of patients with depression compared to the control group. The mean mRNA expression of Foxp3 was considerably reduced in patients suffering from depressive disorders. There was a statistically significant correlation between the number of hospitalizations and the expression of specific inflammatory factors. Conclusions: Expression of specific inflammatory genes may be a factor in the etiopathogenesis of depressive disorders. The duration of the disease seems to be more important for the expression of the genes in question than the severity of depression. These cytokines may affect the metabolism of neurotransmitters and neuroendocrine functions in the brain as well as be a marker and a new potential therapeutic target for recurrent depressive disorders. View Full-Text
Keywords: depression; MDD; autoimmunity; inflammation; interleukin 17 (IL-17); interleukin 21 (IL-21); interleukin 23 (IL-23); interleukin 35 (IL-35); Foxp3; psychiatry; mental disorders; neuroscience; psychiatry depression; MDD; autoimmunity; inflammation; interleukin 17 (IL-17); interleukin 21 (IL-21); interleukin 23 (IL-23); interleukin 35 (IL-35); Foxp3; psychiatry; mental disorders; neuroscience; psychiatry
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MDPI and ACS Style

Gałecka, M.; Bliźniewska-Kowalska, K.; Orzechowska, A.; Szemraj, J.; Maes, M.; Berk, M.; Su, K.-P.; Gałecki, P. Inflammatory versus Anti-Inflammatory Profiles in Major Depressive Disorders—The Role of IL-17, IL-21, IL-23, IL-35 and Foxp3. J. Pers. Med. 2021, 11, 66. https://doi.org/10.3390/jpm11020066

AMA Style

Gałecka M, Bliźniewska-Kowalska K, Orzechowska A, Szemraj J, Maes M, Berk M, Su K-P, Gałecki P. Inflammatory versus Anti-Inflammatory Profiles in Major Depressive Disorders—The Role of IL-17, IL-21, IL-23, IL-35 and Foxp3. Journal of Personalized Medicine. 2021; 11(2):66. https://doi.org/10.3390/jpm11020066

Chicago/Turabian Style

Gałecka, Małgorzata, Katarzyna Bliźniewska-Kowalska, Agata Orzechowska, Janusz Szemraj, Michael Maes, Michael Berk, Kuan-Pin Su, and Piotr Gałecki. 2021. "Inflammatory versus Anti-Inflammatory Profiles in Major Depressive Disorders—The Role of IL-17, IL-21, IL-23, IL-35 and Foxp3" Journal of Personalized Medicine 11, no. 2: 66. https://doi.org/10.3390/jpm11020066

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