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Vuilleumier, N.

Publications and source records attributed to Vuilleumier, N..

2 recordsLinked to original sources

Serum Calprotectin as predictor of Rheumatoid Arthritis disease severity and Mortality

Objective: To evaluate the clinical utility of serum calprotectin (sCAL) as a biomarker of disease activity, disease severity, cardiovascular risk, and mortality in inflammatory rheumatic diseases (IRDs). Methods: Serum calprotectin was measured in 2677 patients with IRDs, including 1472 rheumatoid arthritis (RA), 771 axial spondyloarthritis (axSpA), and 434 psoriatic arthritis (PsA) patients enrolled in the Swiss Clinical Quality Management in Rheumatic Diseases registry, as well as 248 healthy blood donors. Associations with disease activity, radiographic progression, cardiovascular biomarkers, incident major adverse cardiovascular events (MACE), and mortality were evaluated using receiver operating characteristic, Cox regression, and Kaplan-Meier models. Results: sCAL concentrations were significantly higher in RA than in axSpA, PsA, or healthy blood donors. Although diagnostic discrimination between IRDs was modest (Area under the curve (AUC): 0.56), elevated sCAL identified a subset of patients with RA characterized by higher disease activity, higher autoantibody levels, and accelerated radiographic progression, performing better than CRP for the assessment of inflammatory activity, particularly for the discrimination of active synovitis (SJC28[≥]4, AUC 0.67 vs 0.62, p=0.012), even in patients with normal CRP concentrations. Elevated sCAL was independently associated with increased all-cause mortality (HR:2.99; 95% confidence interval (95%CI):1.87-4.78), cardiovascular mortality (HR:7.49;95%CI:1.50-37.55), respiratory mortality (HR: 5.89; 95%CI:1.97-17.62), and incident MACE (HR: 2.10; 95%CI: 1.04-4.24). Furthermore, sCAL correlated with high-sensitivity cardiac troponin T and NT-proBNP concentrations, independently of lipid profile. Conclusions: Serum calprotectin is a clinically relevant biomarker in RA that reflects both disease activity and severity, independently identifying patients at increased cardiovascular risk and mortality, supporting its potential role in disease monitoring and risk stratification.

immunology↗

GPR55 in B cells limits atherosclerosis development and regulates plasma cell maturation

Identifying novel pathways regulating the adaptive immune response in chronic inflammatory diseases such as atherosclerosis is of particular interest in view of developing new therapeutic drugs. Here we report that the lipid receptor GPR55 is highly expressed by splenic B cells and inversely correlates with atheroma plaque size in mice. In human carotid endarterectomy specimen, GPR55 transcript levels were significantly lower in unstable compared to stable carotid plaques. To study the impact of GPR55 deficiency in atherosclerosis, we crossed Gpr55 knockout mice with apolipoprotein E (ApoE) knockout mice and subjected the mice to Western diet for 4 to 16 weeks. Compared to ApoE-/- controls, ApoE-/-Gpr55-/- mice developed larger plaques with increased necrotic core size, associated with elevated circulating and aortic leukocyte counts. Flow cytometry, immunofluorescence and RNA-sequencing analysis of splenic B cells in these mice revealed a hyperactivated B cell phenotype with disturbed plasma cell maturation and immunoglobulin (Ig)G antibody overproduction. The specific contribution of B cell GPR55 in atherosclerosis was further studied in mixed Gpr55-/-/{micro}MT bone marrow chimeras on low density receptor deficiency (Ldlr-/-) background, revealing that B-cell specific depletion of Gpr55 was sufficient to promote plaque development. Conversely, adoptive transfer of wildtype B cells into ApoE-/-Gpr55-/- mice blunted the proatherogenic phenotype. In vitro stimulation of splenocytes with the endogenous GPR55 ligand LPI promoted plasma cell proliferation and enhanced B cell activation marker expression, which was inhibited by the GPR55 antagonist CID16020046. Collectively, these discoveries provide new evidence for GPR55 as key modulator of the adaptive immune response in atherosclerosis. Targeting GPR55 could be useful to limit inflammation and plaque progression in patients suffering from atherosclerosis.

immunology↗