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Immunological subtypes of depression: insights from monocyte gene expression

ABSTRACT: Immunological subtypes of depression: insights from monocyte gene expression

PROVIDER: PRJNA615654 | ENA |

REPOSITORIES: ENA

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Immunological subtypes of depression: insights from monocyte gene expression III

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Immunological subtypes of depression: insights from monocyte gene expression

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Investigating the first genomic response to stress – insights into the etiology and pathophysiology of major depression

Project description:While exposure to adverse life events and subsequent dysregulation of the stress hormone response broadly confer risk for depression, the specific molecular mechanisms mediating this risk are poorly understood. Through pharmacologic activation of the stress hormone response in blood cells we demonstrate that common genetic variants in long-range enhancer elements moderate the immediate transcriptome response to stress, and that these genetic differences are associated with increased risk for depression in the context of early adversity. Using imaging genetics we then link these common risk variants with dysregulated amygdala reactivity, an important trigger of the stress hormone response. The transcripts regulated by these risk variants in peripheral blood were also responsive to stress and stress hormone receptor activation in murine brain. Network modeling approaches suggest that these differences in transcriptional activation may mediate stress-related risk for depression by altering a functional gene network related to proteasome degradation and synaptic plasticity. A Dexamethasone Suppression Test was performed in 160 male subjects. Baseline and stimulated (3 hours after 1.5 mg dexamethasone p.o.) whole blood samples were analyzed using Illumina Human HT-12 v3 arrays.

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Project description:Background: Depressive disorder in adolescents is a clinically heterogeneous condition with poorly defined molecular underpinnings. Glycosylation, a key post-translational modification involved in immune and neuronal regulation, has not been systematically studied across depressive subtypes in youth. Methods: We employed liquid chromatography-tandem mass spectrometry (LC-MS/MS) combined with site-specific glycoproteomic profiling to analyze serum samples from adolescents diagnosed with major depressive disorder, stratified into three subtypes: depression, depression with non-suicidal self-injury (NSSI), and depression with suicide attempts. Healthy adolescents served as controls. Intact N-glycopeptides were quantified to identify subtype-specific glycosylation patterns. Results: Distinct alterations in serum N-glycosylation were observed across depressive subtypes. All groups exhibited decreased levels of bi-antennary glycans and LacNAc/Lewis structures, alongside elevated expression of tetra-antennary sialylated glycans, particularly N6H7S4. NSSI cases showed increased tri-antennary sialylation, while suicidal depression was marked by specific upregulation of N6H7S4 on ORM2. Differentially glycosylated proteins, including SERPING1 and A2M, were enriched in immune, complement, and coagulation pathways. These changes occurred independently of total protein abundance, indicating glycan-specific dysregulation. Conclusion: Our findings uncover subtype-dependent N-glycosylation signatures in adolescent depression and implicate glycan-mediated immune and inflammatory mechanisms in disease heterogeneity. Glycoproteomic profiling offers new insights into biomarker discovery and the molecular classification of depressive subtypes.

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Functional evaluation of neutrophil of patients at high risk for infection treated with monocyte/ neutrophil apheresis

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