BNIP3 deletion ameliorated enterovirus 71 infection-induced hand, foot and mouth disease via inhibiting apoptosis, autophagy, and inflammation in mice.

BNIP3 deletion ameliorated enterovirus 71 infection-induced hand, foot and mouth disease via inhibiting apoptosis, autophagy, and inflammation in mice. Int Immunopharmacol. 2020 Jul 24;87:106799 Authors: Zhu L, Hao X, Cao J, Xie X, Wang H Abstract Bcl2/adenovirus E1B protein-interacting protein 3 (BNIP3) plays a key role in cellular response to stress by regulating apoptosis and selective autophagy. The present study aimed to determine the effects of BNIP3 on enterovirus (EV) 71 infection-induced hand, foot and mouth disease (HFMD), and the apoptosis, autophagy and inflammatory in mice and SH-SY5Y human neuroblastoma cell line. Neonatal BALB/c mice were injected with EV 71 strain to induce the HFMD. Western blotting and ELISA were used to measure the protein expression and cytokine levels. The BNIP3 mRNA and protein levels in the brain were increased in EV 71-infected mice. By contrast, the BNIP3-knockout (KO) mice with EV 71 infection had higher health score and survival rate. BNIP3 deletion reversed the increase of cleaved-caspase 3, cleaved-caspase 8, Bax, LC3 II and LC3 II/LC3 I levels, and the decrease of Bcl2 and Bcl2/Bax and LC3 I levels in the brain of mice with EV 71 infection. The EV 71 infection-induced increase of tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, interleukin (IL)-1β, IL-6, interferon (IFN)-α and IFN-γ levels were inhibited in BNIP3-KO mice. BNIP3 knockdown with small interfering RNA...
Source: International Immunopharmacology - Category: Allergy & Immunology Authors: Tags: Int Immunopharmacol Source Type: research