RESULTS: In this study, the effect of pBD2 on the expression of genes in the TLRs signaling pathway was investigated after IPEC-J2 cells were challenged with E. coli. The results showed that pBD2 decreased the expression of IL-8 induced by E. coli (P < 0.05), and pBD2 significantly decreased the expression of TLR4, TLR5 and TLR7 (P < 0.05), as well as the key downstream genes p38 and JNK which activated by E. coli (P < 0.05). In addition, pBD2 inhibited the p-p65, p-p38 and p-JNK which were up-regulated by E. coli.
CONCLUSIONS: pBD2 could reduce the inflammatory response induced by E. coli perhaps by inhibiting the TLRs-TAK1-NF-κB/MAPK signaling pathway which was activated by E. coli in IPEC-J2 cells. Our study further reveals the immunomodulatory activity of recombinant pBD2 against E. coli, and provides insights into the molecular mechanisms that protect cells from E. coli infection.
结果:在这项研究中,在用大肠杆菌攻击IPEC-J2细胞后,研究了pBD2对TLRs信号通路中基因表达的影响。结果表明,pBD2降低了大肠杆菌诱导的IL-8的表达(P<0.05),pBD2显著降低TLR4、TLR5和TLR7的表达(P<0.05),以及大肠杆菌激活的关键下游基因p38和JNK(P<0.05)。此外,pBD2抑制由大肠杆菌上调的p-p65、p-p38和p-JNK。
结论:pBD2可能通过抑制大肠杆菌在IPEC-J2细胞中激活的TLRs-TAK1-NF-κB/MAPK信号通路来减轻大肠杆菌诱导的炎症反应。我们的研究进一步揭示了重组pBD2对大肠杆菌的免疫调节活性,并提供了保护细胞免受大肠杆菌感染的分子机制的见解。