Inflammatory pathways predict antidepressant treatment non-response among individuals with major depression; yet, this phenomenon may have broader transdiagnostic and transtherapeutic relevance. Among trauma-exposed mothers (M_age=32 years) and their young children (M=4 years), we tested whether genomic and proteomic biomarkers of pro-inflammatory imbalance prospectively predicted treatment response (PTSD and depression) to an empirically-supported behavioral treatment. Forty-three mother-child dyads without chronic disease completed Child Parent Psychotherapy (CPP) for roughly 9 months. Maternal blood was drawn pre-treatment, CD14+ monocytes isolated, gene expression derived from RNA sequencing (n=34; Illumina HiSeq 4000; TruSeq cDNA library), and serum assayed (n=43) for C-Reactive Protein (CRP) and interleukin-1ß (IL-1ß). Symptoms of PTSD and depression decreased significantly from pre- to post-treatment for both mothers and children (all p’s<.01). Nonetheless, a higher pre-treatment maternal pro-inflammatory imbalance of M1-like versus M2-like macrophage-associated RNA expression (M1/M2)(ß=.476, p=.004) and IL-1ß (ß=.333, p=.029), but not CRP, predicted lesser improvements in maternal PTSD symptoms, unadjusted and adjusting for maternal age, BMI, ethnicity, antidepressant use, income, education, and US birth. Only higher pre-treatment M1/M2 predicted a clinically-relevant threshold of PTSD non-response among mothers (OR=3.364, p=.015; ROC-AUC=.78). Additionally, higher M1/M2 predicted lesser decline in maternal depressive symptoms (ß=.556, p=.001), though not independent of PTSD symptoms. For child outcomes, higher maternal IL-1ß significantly predicted poorer PTSD and depression symptom trajectories (ß’s=.318-.429, p’s<.01), while M1/M2 and CRP were marginally associated with poorer PTSD symptom improvement (ß’s=.295-.333, p’s<.056). Pre-treatment pro-inflammatory imbalance prospectively predicts poorer transdiagnostic symptom response to an empirically-supported behavioral treatment for trauma-exposed women and their young children.

炎症通路预测重度抑郁症患者的抗抑郁治疗无反应；然而，这种现象可能具有更广泛的跨诊断和跨治疗相关性。在暴露于创伤的母亲（M_年龄= 32 岁）及其幼儿（M = 4 岁）中，我们测试了促炎失衡的基因组和蛋白质组学生物标志物是否前瞻性地预测了对经验支持的行为的治疗反应（PTSD 和抑郁症）治疗。四十三个没有慢性病的母子完成了大约 9 个月的儿童父母心理治疗 (CPP)。采集母体血液进行预处理，分离 CD14+ 单核细胞，基因表达源自 RNA 测序（n=34；Illumina HiSeq 4000； TruSeq cDNA 文库）和血清测定（n=43）的 C 反应蛋白 (CRP) 和白细胞介素-1ß (IL-1ß)。从治疗前到治疗后，母亲和儿童的 PTSD 和抑郁症状显着下降（所有 p <.01）。尽管如此，M1 样与 M2 样巨噬细胞相关 RNA 表达 (M1/M2) ( ß =.476, p =.004) 和 IL-1ß ( ß =.333 ) 的治疗前母体促炎失衡较高, p =.029)，但不是 CRP，预测产妇 PTSD 症状改善较小，未调整和调整产妇年龄、BMI、种族、抗抑郁药使用、收入、教育和美国出生。只有较高的治疗前 M1/M2 预测了母亲中 PTSD 无反应的临床相关阈值（OR=3.364，p =.015; ROC-AUC=.78)。此外，较高的 M1/M2 预示着产妇抑郁症状的下降幅度较小 ( ß =.556, p =.001)，尽管并非独立于 PTSD 症状。对于儿童结局，较高的母体 IL-1ß 显着预测较差的 PTSD 和抑郁症状轨迹（ß's =.318-.429，p 's<.01），而 M1/M2 和 CRP 与较差的 PTSD 症状改善轻微相关（ß's =.295-.333，p <.056)。治疗前的促炎失衡可以前瞻性地预测对创伤暴露妇女及其幼儿的经验支持的行为治疗的跨诊断症状反应较差。