Serum of Bipolar Patients Induces Pro-inflammatory Activation of Macrophages

2017 ◽  
Vol 41 (S1) ◽  
pp. S114-S114
Author(s):  
S. Dubou Serafim ◽  
P. Ferrari ◽  
R. Colombo ◽  
L. Paul Géa ◽  
M. Migliorini Parisi ◽  
...  

IntroductionEvidence has suggested that immune imbalance is involved with bipolar disorder (BD); however, its precise mechanism is poorly understood.ObjectiveThis study investigated whether biochemical changes in the serum from BD patients could modulate the phenotype of macrophages.MethodsEighteen subjects with BD and healthy individuals (n = 5) were included in this study. The human monocyte cell line U-937 was activated with PMA (phorbol 12-myristate 13-acetate) and polarization was induced with RPMI-1640 media supplemented with 10% serum from each patient for 24 h. Gene expression of selected M1 and M2 markers was assessed by qPCR.ResultsMacrophages exposed to serum of manic and depressive BD patients displayed an increase of IL-1β (6.40 ± 3.47 and 9.04 ± 5.84 versus 0.23 ± 0.11; P < 0.05) and TNF-α (2.23 ± 0.91 and 2.03 ± 0.45 versus 0.62 ± 0.24; P = 0.002 and P = 0.004, respectively) compared to remitted group. In parallel, U-937 macrophages treated with serum of patients in acute episode displayed a down-regulation of CXCL9 (0.29 ± 0.20 versus 1.86 ± 1.61; P = 0.006) and CXCL10 expression (0.36 ± 0.15 and 0.86 ± 0.24 versus 1.83 ± 0.88; P < 0.000 and P = 0.04) compared to remitters.ConclusionsOur 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 can be involved in the etiology of BD.Disclosure of interestThe authors have not supplied their declaration of competing interest.

1986 ◽  
Vol 16 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Charles Félix Calvo ◽  
Shinichiro Watanabe ◽  
Didier Mètivier ◽  
Anna Senik

2000 ◽  
Vol 6 (S2) ◽  
pp. 668-669
Author(s):  
C.S. Little ◽  
A. Maclntyre ◽  
C. Hammond ◽  
E. Venuti ◽  
B.J. Bromke ◽  
...  

Previously, we uncovered evidence of an infectious agent, Chlamydia pneumoniae, associated with sporadic Alzheimer's disease (AD). We demonstrated that C. pneumoniae was present in 90% of brain materials examined from AD patients, compared with 5% in age-matched, non-AD patients. We further showed that microglia and astroglia in the CNS are host cells for the bacterium. RT-PCR analyses indicated that the bacterium is metabolically-active in the brain and could be cultured in a human monocyte cell line (THP-1). Importantly, we showed that the organism is concentrated in areas of AD-neuropathology also containing tau and beta-amyloid. The present study was designed to investigate the effects of C. pneumoniae infection on beta amyloid production in human monocytes (THP-1), astroglial (CCF-STTG1), epithelial (Hep 2), and endothelial (HBMEC) cell lines. We investigated the host pathogen relationship with C. pneumoniae and whether entities characteristic of AD neuropathology such as betaamyloid are associated directly with this infectious agent.


2006 ◽  
Vol 19 (3) ◽  
pp. 546-557 ◽  
Author(s):  
Anthony L. Farone ◽  
Sean M. O'donnell ◽  
Chad S. Brooks ◽  
Kristel M. Young ◽  
Janene M. Pierce ◽  
...  

1989 ◽  
Vol 21 (11) ◽  
pp. 1287-1294 ◽  
Author(s):  
Yukioka Kazuhiko ◽  
Otani Shuzo ◽  
Matsui-Yuasa Isao ◽  
Goto Hitoshi ◽  
Tahara Hideki ◽  
...  

Cytoskeleton ◽  
2011 ◽  
Vol 68 (2) ◽  
pp. 125-137 ◽  
Author(s):  
Maria Antonia Meloni ◽  
Grazia Galleri ◽  
Giuseppe Pani ◽  
Angela Saba ◽  
Proto Pippia ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document