Cyanidin-3-glucoside attenuates silica-induced pulmonary inflammatory responses by modulating T cell immune responses and STAT1/STAT3 signaling

Abstract

• C3G alleviates silica particle-induced pulmonary inflammatory responses in mice. • C3G inhibits silica particle-induced lung T cell accumulation (helper/reg/cytotoxic). • Underlying C3G immune response mechanism likely involves STAT1/STAT3 signaling. Cyanidin-3-glucoside (C3G) is an abundant anthocyanin that exhibits antimicrobial, cardioprotective, and hepatoprotective effects. We applied C3G to silica-injured mice to investigate the efficacy of dietary C3G on lung inflammation and the underlying action mechanism as this information is currently unavailable. We found that C3G treatment significantly alleviated lung inflammation and reduced inflammatory cell infiltration into the lungs. It also reduced the pro-inflammatory cytokine levels in bronchoalveolar lavage fluid. Flow cytometry analysis revealed that C3G treatment ameliorated pulmonary helper and cytotoxic T cell immune responses by decreasing cytokine levels. Regulatory T cells and IL-17A producing-regulatory T cells were also decreased by C3G treatment. Furthermore, C3G effectively suppressed SP-induced activation of the STAT1 and STAT3 signaling pathways of lung tissues. These results demonstrated that dietary C3G could alleviate SP induced lung injury in mice and support the use of C3G as functional food to modulate pulmonary immune responses to silica particles.