Abstract
INTRODUCTION: Major depressive disorder (MDD) is a debilitating disease possibly linked to immune defense mechanisms. TNIP1, a key anti-inflammatory regulator in NF-κB and TLR pathways, is implicated in MDD, but its transcriptional regulation and role in treatment response are unclear. METHODS: We analyzed mRNA expression of TNIP1 and 13 transcription factors in monocytes from pre- and post-treatment (4-6 weeks) MDD patients and healthy controls. Peripheral blood mononuclear cells were isolated, tagged by CD14, and mRNA was extracted and analyzed. Participants were recruited at Kaohsiung Chang Gung Memorial Hospital (2014-2025). ANCOVA, paired t-tests, and multiple linear regression adjusted for age, gender, BMI, and smoking were used to compare groups and predict treatment outcomes. RESULTS: This study encompassed 62 MDD patients and 52 healthy controls. Pre-treatment HAMD-17 averaged 23.90 ± 4.60, and post-treatment HAMD-17 averaged 8.43 ± 4.24. MDD patients showed higher PPAR-γ (p < 0.001), FOS (p = 0.023), and lower JUN (p = 0.029) expression than controls. Post-treatment, TNIP1 expression increased (p = 0.031). Lower pre-treatment PPAR-γ predicted greater symptom improvement (p = 0.016). CONCLUSION: This study highlights the differential expression of PPAR-γ, FOS, and JUN in MDD patients, underscoring their potential roles in immune regulation. The association between lower pre-treatment PPAR-γ expression and improved treatment outcomes suggests its utility as a biomarker for predicting therapeutic response.