Key result
Enterovirus 71 induces GSDMD/NLRP3-mediated pyroptosis of human neuroblastoma SH-SY5Y cells through up-regulation of miR-146a and subsequent down-regulation of its target CXCR4.
Why the study?
Enterovirus 71 tends to induce severe neurological complications and death, but the detailed mechanism causing nervous system disorders remains unclear.
Does Enterovirus 71 induce pyroptosis in human neuroblastoma SH-SY5Y cells through the miR-146a/CXCR4 axis?
Does Enterovirus 71 induce pyroptosis in human neuroblastoma SH-SY5Y cells through the miR-146a/CXCR4 axis?
EV71 induces nervous system cell damage through regulating miR-146a/CXCR4 mediated pyroptosis, revealing a potential mechanism for EV71-induced neurological complications.
Findings remain preclinical; leaves open miR-146a/CXCR4 as a target for EV71 neurological complications.
Enterovirus 71 (EV71) is a predominant causative pathogen of hand-foot-and-mouth disease (HFMD) in children. Compared with other HFMD-associated viruses, EV71 tends to induce more severe neurological complications and even death. However, the detailed mechanism of EV71 causes nervous system disorder is still unclear. In this study, we found that EV71 induced the GSDMD/NLRP3-mediated pyroptosis of SH-SY5Y cells through up-regulated miR-146a. Through bioinformatic analysis, we identified C-X-C chemokine receptor type 4 (CXCR4) as the potential target of miR-146a. We noticed that the expression of CXCR4 was regulated by miR-146a during EV71 infection. Moreover, our results show that over-expression of CXCR4 attenuated EV71-induced pyroptosis of SY-SY5Y cells. These results reveal a previously unrecognized mechanism in which EV71 induces nervous system cells damage through regulating miR-146a/CXCR4 mediated pyroptosis.
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Guo et al. (2023) studied Enterovirus 71 infection. Enterovirus 71 infection was evaluated on GSDMD/NLRP3-mediated pyroptosis. Enterovirus 71 induces GSDMD/NLRP3-mediated pyroptosis of human neuroblastoma SH-SY5Y cells through up-regulation of miR-146a and subsequent down-regulation of its target CXCR4.
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