MiR-210 suppresses Candida albicans-derived β-glucan-induced inflammation in THP-1-derived macrophages via the Syk-NF-κB pathway.

In immunocompromised individuals, infections due to Candida albicans (C. albicans) can be life-threatening. Recognition of the insoluble β-glucan derived from the C. albicans cell wall (CaIG) by Dectin-1 in macrophages initiates an inflammatory reaction that is critical for clearing the fungal infection. However, uncontrolled inflammation may lead to septic shock. Research has established that miR-210 is strongly upregulated in THP-1-derived macrophages (THP-1 macrophages) following CaIG stimulation. MiR-210 has been implicated in the metabolic and immunological responses of macrophages in various infectious and inflammatory disease models. Nevertheless, whether miR-210 modulates Dectin-1-activated inflammation remains unclear. An in vitro inflammation model was established using CaIG-stimulated THP-1 macrophages in the current research. By using miR-210 mimic and inhibitor transfection approaches, we observed that miR-210 overexpression significantly reduced CaIG-induced IL-6 and TNF-α expression, whereas inhibition of endogenous miR-210 enhanced their production. Furthermore, by inhibiting CaIG-triggered spleen tyrosine kinase (Syk) activation and subsequent IκBα phosphorylation, miR-210 effectively prevents the accumulation of NF-κB p65 in the nucleus in THP-1 macrophages. These findings demonstrate that miR-210 participates in negative feedback to limit CaIG-triggered inflammation, primarily through downregulating the Syk-NF-κB signaling cascade. In summary, our findings reveal that miR-210 acts as a precise inflammatory modulator in macrophages, highlighting its therapeutic potential.