Chen W, Liu Z, Zhang Q, Yan Q, Jing S
Acta Virol. 2018;62(3):287-293. doi: 10.4149/av_2018_222.
Antimicrobial peptides produced by epithelial and immune cells protect tissues from various infections. Whether enterovirus infection leads to stimulation of antimicrobial peptide expression is unknown. We examined antimicrobial peptide mRNA and protein production in HT-29 colon adenocarcinoma cells infected with picornaviruses. The antiviral activity of increased antimicrobial peptide production was evaluated by using a recombinant peptide and corresponding gene overexpression. Enterovirus infection enhanced both the mRNA expression and secretion of human β-defensin (hBD) 3 in intestinal epithelial cells but did not increase expression of human neutrophil peptide 1-3 (HNP 1-3), HNP4, human defensin 5 (HD5), HD6, hBD1, hBD2, and hBD5. The recombinant but not the intracellularly overexpressed hBD3 inhibited enterovirus (EV) 71, coxsackievirus A16 (CVA16), CVB5 and poliovirus 1 (PV1) infecting HT-29 cells. Our results suggest that enterovirus infection induces hBD3 production in human intestinal epithelial cells and that hBD3 can exert extracellular anti-enterovirus activity.
上皮细胞和免疫细胞产生的抗菌肽可保护组织免受各种感染。肠道病毒感染是否会刺激抗菌肽表达尚不清楚。我们检测了感染小核糖核酸病毒的HT - 29结肠腺癌细胞中抗菌肽的mRNA和蛋白质产生情况。通过使用重组肽和相应基因过表达来评估抗菌肽产量增加的抗病毒活性。肠道病毒感染增强了肠道上皮细胞中人β - 防御素（hBD）3的mRNA表达和分泌，但未增加人中性粒细胞肽1 - 3（HNP 1 - 3）、HNP4、人防御素5（HD5）、HD6、hBD1、hBD2和hBD5的表达。重组的而非细胞内过表达的hBD3抑制感染HT - 29细胞的肠道病毒（EV）71、柯萨奇病毒A16（CVA16）、CVB5和脊髓灰质炎病毒1（PV1）。我们的结果表明，肠道病毒感染可诱导人肠道上皮细胞产生hBD3，且hBD3可发挥细胞外抗肠道病毒活性。
