BMC psychiatry · 2026
Elevated serum calprotectin levels in major depressive disorder: no evidence of association with S100A9 rs3014866 polymorphism.
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Akbas Furkan, Baykan Ozgur, Avcikurt Ayla Solmaz, Baykan Hayriye
Аннотация
BACKGROUND: Major depressive disorder (MDD) has been increasingly associated with low-grade inflammation, with neutrophils playing a central role. Calprotectin is a mainly neutrophil-derived inflammatory mediator. We investigated whether serum calprotectin levels are higher in patients with MDD than in healthy controls and whether the S100A9 rs3014866 polymorphism is associated with serum calprotectin levels and with MDD.
METHODS: We enrolled 66 patients with major depressive disorder (MDD) and 54 healthy controls. Depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HAM-D). Fasting venous blood samples were collected to measure serum calprotectin and to genotype the S100A9 rs3014866 polymorphism.
RESULTS: Serum calprotectin levels were higher in patients with MDD than in healthy controls (2.18 ± 1.33 vs. 1.05 ± 0.55 µg/mL; p < 0.001). Serum calprotectin levels were positively correlated with HAM-D scores among patients with MDD (rs = 0.314, p = 0.010). The S100A9 rs3014866 genotype distribution was in Hardy-Weinberg equilibrium. Genotype and allele frequencies did not differ significantly between patients with MDD and healthy controls, and serum calprotectin levels did not differ significantly across genotype groups under the tested inheritance models.
CONCLUSIONS: These findings suggest that serum calprotectin may reflect inflammatory processes associated with MDD and that its potential role as a biomarker warrants further investigation.
METHODS: We enrolled 66 patients with major depressive disorder (MDD) and 54 healthy controls. Depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HAM-D). Fasting venous blood samples were collected to measure serum calprotectin and to genotype the S100A9 rs3014866 polymorphism.
RESULTS: Serum calprotectin levels were higher in patients with MDD than in healthy controls (2.18 ± 1.33 vs. 1.05 ± 0.55 µg/mL; p < 0.001). Serum calprotectin levels were positively correlated with HAM-D scores among patients with MDD (rs = 0.314, p = 0.010). The S100A9 rs3014866 genotype distribution was in Hardy-Weinberg equilibrium. Genotype and allele frequencies did not differ significantly between patients with MDD and healthy controls, and serum calprotectin levels did not differ significantly across genotype groups under the tested inheritance models.
CONCLUSIONS: These findings suggest that serum calprotectin may reflect inflammatory processes associated with MDD and that its potential role as a biomarker warrants further investigation.