Disruptions of p11 (S100A10) and HPA Axis Homeostasis Participate in the Major Depressive Disorder (MDD) Especially...

Patients suffering from major depressive disorder (MDD) commonly exhibit abnormal p11 (S100A10) and dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) axis. This study was aimed to quantify peripheral p11, cortisol (COR), and adrenocorticotropic hormone (ACTH) levels and further revealed the possible mechanisms of MDD and antidepressant response.

A total of 60 MDD inpatients and 67 healthy controls (HC) were recruited in this study. Demographic characteristics and neuropsychological assessment including Hamilton rating scale for depression-17 (HAMD-17), Hamilton anxiety rating scale (HAMA), Snaith-Hamilton pleasure scale (SHAPS) and temporal experience of pleasure scale (TEPS) were collected. A main antidepressant was utilized after the patients were enrolled (T0) and at two week follow-up (T2). Peripheral p11 levels including monocyte (MO), natural killer (NK), T-cell, COR, and ACTH were measured by multicolor flow cytometry and enzyme-linked immunosorbent assay at T0 and T2.

CD4+T p11, COR and ACTH were significantly different between the MDD and HC groups at T0 (all P < 0.05). Subgroup analysis by gender showed that the MO-C, MO-NC, and NK p11+ cells were higher in female than in male MDD patients (all P < 0.05). There was a negative relationship between p11 of MO-NC, CD4+T, CD8+T, and TEPS. However, there was no significant difference between T0 and T2 in MDD patients.

Baseline p11 levels may serve as a peripheral blood biomarker for female depressive patients and further provide more insight into the pathological mechanisms of MDD.