Fucosylated oligosaccharide Lacto-N-fucopentaose I ameliorates enterovirus 71 infection by inhibiting apoptosis

Abstract

Enterovirus 71 (EV71) is the main cause of hand, foot and mouth disease that results in high rates of severe diseases in small children. Lacto-N-fucopentaose I (LNFPI) can inhibit pathogen invasion and regulate intestinal flora. However, whether LNFPI inhibits EV71 infection remains unknown. In this study, we examined the effect and mechanism of LNFPI against EV71. LNFPI reduced capsid protein VP1 to block virus adsorption, inhibited cyclin E transcription and promoted CDK2 expression in EV71-induced human rhabdomyosarcoma cells, thereby causing virus-induced S phase arrest and inhibiting death receptor and mitochondria-induced apoptosis. The effects of LNFPI on apoptosis were further confirmed in Caenorhabditis elegans. The correlation analysis revealed that LNFPI inhibited cell apoptosis by reducing the abundance of Sphingomonas, Stenotrophomonas and Achromatic, which are associated with pro-apoptotic genes in C. elegans, and by increasing the abundance of Micromonospora, which is related to apoptotic inhibition. These findings lead to further recommendations for LNFPI supplementation in infant formula, as it could offer antiviral benefits to formula-fed infants.

Keywords

• Lacto-N-fucopentaose I
• Enterovirus 71
• Cell apoptosis
• Cell cycle
• Intestinal flora