Bombyx mori gloverin A2 (BMGlvA2) is an induced antimicrobial insect protein isolated from Bombyx mori. This study was conducted to explore the effect and potential mechanisms of BMGlvA2 on inflammatory responses and cellular functions in intestinal epithelial cells (IPEC-J2) exposure to enterotoxigenic E. coli (ETEC). IPEC-J2 cells pretreated with or without BMGlvA2 (12.5 μg/mL) were challenged by ETEC K88 (1×10⁶ CFU/well) or culture medium. We show that BMGlvA2 pretreatment increased the cell viability and improved the distribution and abundance of tight junction protein ZO-1 in IPEC-J2 cells exposure to ETEC (P < 0.05). Interestingly, BMGlvA2 not only decreased the expression levels of inflammatory cytokines such as the tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), but also decreased the expression level of Caspase3 and the apoptosis rate in the ETEC-challenged cells (P < 0.05). Importantly, BMGlvA2 decreased the protein abundances of two critical inflammation-associated signaling proteins, phosphorylated nuclear factor-kappa-B inhibitor alpha (p-IκBα) and phosphorylated nuclear factor-kappa B (p-NF-κB), in the ETEC-challenged cells. These results indicate that BMGlvA2 attenuates ETEC-induced inflammation in the IPEC-J2 cells by regulating the NF-κB signaling pathway, resulting in decreased secretion of inflammatory cytokine and reduced cell apoptosis.

Bombyx mori gloverin A2 (BMGlvA2) 是一种从Bombyx mori中分离出来的诱导性抗菌昆虫蛋白。本研究旨在探讨 BMGlvA2 对肠上皮细胞 (IPEC-J2) 暴露于产肠毒素大肠杆菌(ETEC) 的炎症反应和细胞功能的影响和潜在机制。用或不用BMGlvA2（12.5 μg/mL）预处理的IPEC-J2细胞用ETEC K88（1×10 ⁶  CFU/孔）或培养基攻击。我们表明 BMGlvA2 预处理增加了细胞活力并改善了 IPEC-J2 细胞中紧密连接蛋白 ZO-1 的分布和丰度暴露于 ETEC ( P < 0.05)。有趣的是，BMGlvA2不仅降低了肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）等炎性细胞因子的表达水平，而且降低了ETEC中Caspase3的表达水平和细胞凋亡率。 -挑战细胞（P  < 0.05）。重要的是，BMGlvA2 降低了 ETEC 挑战中两种关键的炎症相关信号蛋白，磷酸化核因子-kappa-B 抑制剂 α (p-IκBα) 和磷酸化核因子-kappa B (p-NF-κB) 的蛋白质丰度。细胞。这些结果表明，BMGlvA2 通过调节 NF-κB 信号通路减弱 ETEC 诱导的 IPEC-J2 细胞炎症，导致炎性细胞因子分泌减少和细胞凋亡减少。