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Published on: November 30, 2015
Plasma complement C3 and C3a are increased in major depressive disorder independent of childhood trauma
Xianmei Luo1,2, Zeman Fang1, Lingyun Lin1
1Mental Health Center of Shantou University, Mental Health Center, Taishan North Road, Shantou, 515065, China.
Insights
Elevated complement C3 and C3a levels are linked to major depressive disorder (MDD) pathophysiology. However, childhood trauma history did not correlate with these inflammatory markers in MDD patients.
Area of Science:
- Neuroimmunology
- Psychiatry
Background:
- The complement system plays a role in major depressive disorder (MDD) pathophysiology.
- Childhood trauma may increase adult depression risk through immune activation.
Purpose of the Study:
- To compare peripheral levels of complement C3, C3a, C1q, and C-reactive protein (CRP) in MDD patients and healthy controls.
- To investigate the association between these molecule levels and childhood trauma history in MDD patients.
Main Methods:
- Recruited 49 medication-free MDD patients and 45 healthy controls.
- Administered the Childhood Trauma Questionnaire and collected blood samples.
- Measured plasma C3, C3a, C1q, and CRP using enzyme-linked immunosorbent assay.
Main Results:
- MDD patients showed significantly higher plasma concentrations of C3 and C3a compared to controls.
- Plasma concentrations of C1q and CRP were comparable between MDD patients and controls.
- No association was found between childhood trauma history and the measured inflammatory factors in MDD patients.
Conclusions:
- Complement C3 and C3a may be involved in the pathophysiology of MDD.
- Childhood trauma history was not associated with circulating levels of complement C3, C3a, C1q, and CRP in this cohort.
Background:
Dysregulated complement system is linked to pathophysiology of major depressive disorder (MDD). Childhood trauma has been associated with an increased incidence of adult depression via a putative mechanism of immune activation. This study aimed to measure and compare peripheral levels of complement C3, C3a, C1q and C-reactive protein (CRP) in MDD patients and healthy controls and explore the relationship between these molecule levels and childhood trauma history in the participants.
Methods:
The participants were 49 medication-free MDD patients and 45 healthy controls. All participants were asked to finish the Childhood Trauma Questionnaire, followed by blood sampling for measurement of plasma complement C3, C3a, C1q and CRP by means of enzyme-linked immunosorbent assay.
Results:
Peripheral plasma concentration of C3 and C3a in medication-free MDD group was significantly higher than that in the healthy controls; whereas the concentration of plasma C1q and CRP in depressed patients was comparable to that in healthy controls. All these inflammatory factors were not associated to childhood trauma experience in patients with MDD.
Conclusion:
Our data suggest that complement C3 and C3a may be implicated in the pathophysiology of MDD, although traumatic childhood experiences were not associated with the circulating levels of complement C3, C3a, C1q and CRP.
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