Depression and Mania Induce Pro-inflammatory Activation of Macrophages Following Application of Serum from Individuals with Bipolar Disorder
10.9758/cpn.2018.16.1.103
- Author:
Pamela FERRARI
1
;
Mariana Migliorini PARISI
;
Rafael COLOMBO
;
Matheus BECKER
;
Gabriel FRIES
;
Bruna Maria ASCOLI
;
Luiza Paul GÉA
;
Márcia KAUER-SANT’ANNA
;
Flávio KAPCZINSKI
;
Fábio KLAMT
;
Fátima T C R GUMA
;
Adriane Ribeiro ROSA
;
Florencia M BARBÉ-TUANA
Author Information
1. Laboratory of Molecular Psychiatry, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil. adrianerrosa@gmail.com
- Publication Type:Original Article
- Keywords:
Bipolar disorder;
Cytokines;
Chemokines;
Macrophages;
Polarization;
U-937
- MeSH:
Bipolar Disorder;
Cell Line;
Chemokines;
Cytokines;
Depression;
Down-Regulation;
Gene Expression;
Humans;
Macrophages;
Monocytes;
Mononuclear Phagocyte System;
Necrosis;
Phenotype;
Polymerase Chain Reaction
- From:Clinical Psychopharmacology and Neuroscience
2018;16(1):103-108
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: Evidence has suggested that immune imbalance is involved with bipolar disorder (BD); however, its precise mechanism is poorly understood. This study investigated whether biochemical changes in the serum from BD patients could modulate the phenotype of cultured macrophages. METHODS: Eighteen subjects with BD and five healthy individuals were included in this study. The human monocyte cell line U-937 was activated with phorbol 12-myristate 13-acetate (PMA) and polarization was induced with RPMI-1640 media supplemented with 10% serum from each patient for 24 hours. Gene expression of selected M1 and M2 markers was assessed by quantitative PCR. RESULTS: Macrophages exposed to serum of manic and depressive BD patients displayed an increase of interleukin-1β (6.40±3.47 and 9.04±5.84 vs. 0.23±0.11; p < 0.05) and tumor necrosis factor-α (2.23±0.91 and 2.03±0.45 vs. 0.62±0.24; p=0.002 and p=0.004, respectively) compared to euthymic group (there was no difference between euthymic and controls). In parallel, U-937 macrophages treated with serum of patients in acute episode displayed a down-regulation of CXCL9 (0.29±0.20 vs. 1.86±1.61; p=0.006) and CXCL10 expression (0.36±0.15 and 0.86±0.24 vs. 1.83±0.88; p < 0.000 and p=0.04) compared to the euthymia group. CONCLUSION: Our results are consistent with previous studies showing that changes in peripheral blood markers could modulate M1/M2 polarization in BD. The evidence of macrophages as source of inflammatory cytokines might be helpful to unravel how the mononuclear phagocyte system is involved in the etiology of BD.
