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A Multiomic Analysis to Identify Drivers of Subclinical Vascular Disease in Systemic Lupus Erythematosus
Christopher Oliveira1, Yenealem Temesgen-Oyelakin1, Mohammad Naqi1
1National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Insights
Systemic lupus erythematosus (SLE) is linked to increased cardiovascular disease (CVD) risk. Blood immune signatures and proteins may help identify at-risk patients and develop new CVD biomarkers for lupus.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Genomics
Background:
- Systemic lupus erythematosus (SLE) significantly elevates cardiovascular disease (CVD) risk beyond traditional factors.
- Identifying immunologic signatures associated with subclinical CVD in SLE is crucial for risk stratification.
Purpose of the Study:
- To characterize blood gene expression and serum protein profiles associated with subclinical CVD in SLE patients.
- To identify potential novel biomarkers for CVD risk in SLE.
Main Methods:
- Assessed arterial stiffness (CAVI), vascular inflammation (TBR), and coronary atherosclerosis (NCB) in SLE patients and healthy controls.
- Performed whole blood bulk RNA sequencing and quantified serum inflammatory protein biomarkers using Olink platform.
Main Results:
- SLE patients exhibited increased CAVI, TBR, and noncalcified coronary plaque burden (NCB) compared to controls.
- Gene expression analysis revealed down-regulation in cell cycle and altered metabolism pathways in SLE.
- Specific serum proteins (e.g., IL-33, CCL23, Flt3L) were associated with adverse vascular phenotypes.
Conclusions:
- Blood-based immune and metabolic pathway dysregulation is linked to premature CVD in SLE.
- Identified cytokines and chemokines may serve as novel CVD biomarkers for SLE patients.
Objective:
Systemic lupus erythematosus (SLE) increases cardiovascular disease (CVD) risk, and this is not explained by traditional risk factors. Characterization of blood immunologic signatures that associate with subclinical CVD and predict its progression has been challenging and may help identify subgroups at risk.
Methods:
Patients with SLE (n = 77) and healthy controls (HCs) (n = 27) underwent assessments of arterial stiffness, vascular wall inflammation, and coronary atherosclerosis burden with cardio-ankle vascular index (CAVI); fluorodeoxyglucose-positron emission tomography/computed tomography (CT) (target-to-background ratio [TBR]); and coronary CT angiography. Whole blood bulk RNA sequencing was performed in a subset of study participants (HC n = 10, SLE n = 20). In a partially overlapping subset (HC n = 24, SLE n = 64), serum inflammatory protein biomarkers were quantified with an Olink platform.
Results:
CAVI, TBR, and noncalcified coronary plaque burden (NCB) were increased in patients with SLE compared to HCs. When comparing patients with SLE with high CAVI scores to those with low CAVI scores or to HCs, there was a down-regulation of genes in pathways involved in the cell cycle and differentially regulated pathways related to metabolism. Distinct serum proteins associated with increased CAVI (CCL23, colony-stimulating factor 1, latency-activating peptide transforming growth factor β1, interleukin 33 [IL-33], CD8A, and IL-12B), NCB (monocyte chemotactic protein 4 and FMS-like tyrosine kinase 3 ligand [Flt3L]), and TBR (CD5, IL-1α, AXIN1, cystatin D [CST5], and tumor necrosis factor receptor superfamily 9; P < 0.05).
Conclusion:
Blood gene expression patterns and serum proteins that associate with worse vascular phenotypes suggest dysregulated immune and metabolic pathways linked to premature CVD. Cytokines and chemokines identified in associations with arterial stiffness, inflammation, and NCB in SLE may allow for characterization of new CVD biomarkers in lupus.
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