Protective effect of Bombyx mori gloverin on intestinal epithelial cells exposure to enterotoxigenic E. coli

Abstract

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 (1×10 6 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.

Gut Microbiota Analysis in Silkworms (Bombyx mori) Provides Insights into Identifying Key Bacterials for Inclusion in Artificial Diet Formulations

“…The observed gradual transition in the microbial community's composition, marked by the co-dominance of the Proteobacteria and Actinobacteria phyla, underscores the resilience and adaptability of the gut microbiota. This capacity for adaptation is vital for silkworms to manage the challenges associated with shifting from an artificial to a natural diet, which encompasses adjustments in nutrient composition, digestibility, and the introduction of plant secondary metabolites [22,32].…”

Comprehensive Analysis Revealed the Potential Roles of N6-Methyladenosine (m6A) Mediating E. coli F18 Susceptibility in IPEC-J2 Cells

“…In general, the intestinal porcine epithelial cell (IPEC-J2) is an efficient cell model for the examination of the underlying mechanism behind the host anti- E. coli F18 pathogen [ 7 , 20 ]. In addition, multiple studies have revealed that the IPEC-J2 exposure to E. coli triggers oxidative damage and inflammatory responses, which results in enhancing apoptotic cell death and diminishing functionality [ 21 , 22 , 23 ]. Nevertheless, the explicit biological role of m 6 A regulators in conferring resistance against E. coli F18-based infection in IPEC-J2 cells remains undetermined.…”