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Aim: Several lines of evidence suggest that major depressive disorder is associated with an inflammatory status. Tumor necrosis factor-a has been investigated as a potential molecular target in mood disorders. Tumor necrosis factor-a exerts its activity through binding to specific cell membrane receptors named as TNFR1 and TNFR2. The aim of the present study was to investigate soluble plasma TNFR1 (sTNFR1) and TNFR2 levels (sTNFR2) in major depressive disorder patients.Methods: Female outpatients with major depressive disorder (n = 30) were compared with a healthy control group (n = 19). Severity of depressive symptoms was evaluated on Beck Depression Inventory; post-traumatic stress disorder (PTSD) symptoms were evaluated on PTSD Checklist-Civilian Version; and childhood abuse and neglect on the Childhood Trauma Questionnaire. Plasma tumor necrosis factor-a and its soluble receptors were measured by ELISA. Results: Patients had no changes in tumor necrosisfactor-a concentrations but did have increased sTNFR1 (P < 0.001) and sTNFR2 (P < 0.001) levels compared to controls. Plasma level of sTNFR1 was positively predicted by age (B = 0.25, P = 0.05) and PTSD-like symptoms (B = 0.41, P = 0.002) and plasma levels of sTNFR2 by depression severity (B = 0.67, P < 0.001).Conclusions: Soluble tumor necrosis factor-a receptors could be reliable markers of inflammatory activity in major depression.

The findings of this study indicated that the presence of recurrent MDD with suicidal ideation is associated with differences in inflammatory chemokines when compared to those without suicidal ideation.

Early life stress has been suggested to mediate vulnerability to affective disorders. Traumatic events experienced in childhood such as sexual abuse and/or physical neglect may lead to psychiatric diseases in adult life, including post-traumatic stress disorder (PTSD). Previous studies have focused on adult traumatic events and very little is known regarding the long-term physiological effects of early life stress. Here, we review the complex interplay between most important cognitive, neuroendocrine and immunological changes reported in PTSD, focusing on long-term implications of childhood maltreatment. PTSD has been associated with significant biological changes related to impaired cognitive functions, attenuated hypothalamic-pituitary-adrenal (HPA) axis function (hypocortisolism) and activation of innate immune responses (low-grade inflammation).