Cyanidin 3-O-glucoside Chloride Attenuates Streptococcus suis-Induced Inflammation by Inhibiting MAPK and NF-κB Signaling Pathways in Murine Macrophage J774 Cells.

Abstract

Streptococcus suis serotype 2 (SS2), considered to be the most frequent and virulent type among identified serotypes, is an important emerging or re-emerging zoonotic pathogen. Inflammation is thought to be a hallmark of SS2 infection, as demonstrated by most clinical symptoms varying from an asymptomatic bacteremia to a fulminant systemic disorder. The aim of this study was to investigate whether cyanidin-3-O-glucoside (C3G), a widely distributed anthocyanin, could exert a protective effect against the SS2-mediated inflammatory response, as well as to explore the underlying mechanisms in J774 cells in vitro. The results demonstrated that C3G had little anti-SS2 activity at concentrations ranging from 8-32 μg/mL, whereas it significantly alleviated SS2-induced J774 cell injury. C3G also significantly inhibited the production of pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6) in cell supernatants as determined by enzyme-linked immunosorbent assay. Western blot assays also showed that C3G significantly suppressed SS2-induced activation of the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways by inhibiting the phosphorylation of p38, extracellular signal-regulated kinase (ERK1/2), and Jun-N terminal kinase (JNK1/2), inhibitor κB-α and NF-κB p65 in J774 cells. Our results indicated that C3G may ameliorate SS2-induced cell injury partially resulting from its anti-inflammatory effects by inhibiting the MAPK and NF-κB pathways.