Andre R Brunoni1, Thitiporn Supasitthumrong2, Antonio Lucio Teixeira3, Erica Lm Vieira3, Wagner F Gattaz4, Isabela M Benseñor5, Paulo A Lotufo5, Beny Lafer6, Michael Berk7, Andre F Carvalho8, Michael Maes9. 1. Department of Internal Medicine, Faculdade de Medicina da Universidade de São Paulo & Hospital Universitário, Universidade de São Paulo, Av. Prof Lineu Prestes 2565, 05508-000 São Paulo, Brazil; Laboratory of Neurosciences (LIM-27), Department and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, R Dr Ovidio Pires de Campos 785, 2o andar, 05403-000 São Paulo, Brazil. 2. Department of Psychiatry, Chulalongkorn University, Faculty of Medicine, Bangkok, Thailand. 3. Interdisciplinary Laboratory of Medical Investigation, Faculdade de Medicina da Universidade Federal de Minas Gerais, Brazil; Neuropsychiatry Program, Department of Psychiatry & Behavioral Sciences, UT Health Houston, United States. 4. Laboratory of Neurosciences (LIM-27), Department and Institute of Psychiatry, Faculdade de Medicina da Universidade de São Paulo, R Dr Ovidio Pires de Campos 785, 2o andar, 05403-000 São Paulo, Brazil. 5. Department of Internal Medicine, Faculdade de Medicina da Universidade de São Paulo & Hospital Universitário, Universidade de São Paulo, Av. Prof Lineu Prestes 2565, 05508-000 São Paulo, Brazil. 6. Bipolar Disorder Research Program, Department and Institute of Psychiatry, University of São Paulo Medical School, São Paulo, Brazil. 7. Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, Geelong, Australia; Orygen, The National Centre of Excellence in Youth Mental Health, Centre for Youth Mental Health, Florey Institute for Neuroscience and Mental Health and the Department of Psychiatry, The University of Melbourne, Melbourne, Australia. 8. Department of Psychiatry, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Centre for Addiction & Mental Health (CAMH), Toronto, Canada. Electronic address: andre.carvalho@camh.ca. 9. Department of Psychiatry, Chulalongkorn University, Faculty of Medicine, Bangkok, Thailand; Deakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, Geelong, Australia; Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria.
Abstract
BACKGROUND: Major depressive disorder (MDD) and bipolar depression (BD) both share increased immune-inflammatory activation. However, there are unclear patterns of differences in peripheral immune profiles between them. METHODS: We examined such differences in 245 MDD and 59 BD patients, recruited in the same center, who were in an acute depressive episode of moderate severity. Hierarchical binary logistic regression analyses and generalized linear models were used to compare levels of plasma biomarkers between groups and to predict dichotomous classification. RESULTS: Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, IL-12 and IL-10 were significantly higher in MDD than in BD, whereas IL-6, sTNFR2, IL-18, IL-33, ST2 (IL1R Like 1) and KLOTHO were significantly higher in BD than in MDD. Moreover, logistic regression analyses correctly classified BD and MDD patients with 98.1% accuracy, using a combination of IL-6, IL-8, ST2, sTNFR2 (directly associated with BD) and IL-12 and TNF-α (directly associated with MDD). Patients with MDD with melancholic features showed higher IL-1β levels than those without melancholia. The sTNFR1 / sTNFR2 ratio significantly predicted MDD and state and trait anxiety and negative affect. Results remained significant after covariate adjustment, including drug use. LIMITATIONS: Cross-sectional study. Lack of control comparison group. Differences in exposure to medications among participants. CONCLUSIONS: Differences in immune profiles between BD and MDD patients exist, especially for the compensatory immune-regulatory system (CIRS): increased IL-10 is the primary immune-regulatory mechanism in MDD, while increased sTNFR2 and KLOTHO are the primary regulatory mechanisms in BD.
BACKGROUND: Major depressive disorder (MDD) and bipolar depression (BD) both share increased immune-inflammatory activation. However, there are unclear patterns of differences in peripheral immune profiles between them. METHODS: We examined such differences in 245 MDD and 59 BDpatients, recruited in the same center, who were in an acute depressive episode of moderate severity. Hierarchical binary logistic regression analyses and generalized linear models were used to compare levels of plasma biomarkers between groups and to predict dichotomous classification. RESULTS: Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, IL-12 and IL-10 were significantly higher in MDD than in BD, whereas IL-6, sTNFR2, IL-18, IL-33, ST2 (IL1R Like 1) and KLOTHO were significantly higher in BD than in MDD. Moreover, logistic regression analyses correctly classified BD and MDDpatients with 98.1% accuracy, using a combination of IL-6, IL-8, ST2, sTNFR2 (directly associated with BD) and IL-12 and TNF-α (directly associated with MDD). Patients with MDD with melancholic features showed higher IL-1β levels than those without melancholia. The sTNFR1 / sTNFR2 ratio significantly predicted MDD and state and trait anxiety and negative affect. Results remained significant after covariate adjustment, including drug use. LIMITATIONS: Cross-sectional study. Lack of control comparison group. Differences in exposure to medications among participants. CONCLUSIONS: Differences in immune profiles between BD and MDDpatients exist, especially for the compensatory immune-regulatory system (CIRS): increased IL-10 is the primary immune-regulatory mechanism in MDD, while increased sTNFR2 and KLOTHO are the primary regulatory mechanisms in BD.
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