Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets.
Effects of HSP27 gene expression on the resistance to Escherichia coli infection in piglets.
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DOI：
10.1016/j.gene.2021.145415
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发表时间：
2021-01
期刊：
影响因子：
3.5
通讯作者：
Q. Zong;Pengfei Jing;Shouyong Sun;Haifei Wang;Shenglong Wu;W. Bao
中科院分区：
文献类型：
--
作者：
Q. Zong;Pengfei Jing;Shouyong Sun;Haifei Wang;Shenglong Wu;W. Bao
Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function ofHSP27gene and its regulatory mechanism as infected byEscherichia coli(E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression ofHSP27gene in F18 resistant and sensitive Sutai pigs and the differential expression uponE. coliF18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, theHSP27gene overexpression vector was constructed to detect the effect of theHSP27gene overexpression on the adhesion ofE. coliF18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, theRSK2gene overexpression vector was constructed and the number of colonies was counted after co-transfection ofHSP27andRSK2gene. Results revealed that the expression level ofHSP27gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels ofHSP27gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P< 0.01). The adhesion ability ofE. coliF18ab to IPEC-J2 was significantly reduced afterHSP27gene overexpression (P< 0.01), and the concentration of pro-inflammatory factors in theHSP27gene overexpression group was significantly reduced compared with the control group after F18ab infection (P< 0.05). Furthermore, the expression ofRSK2was significantly increased inHSP27overexpression group upon F18ab infection (P< 0.01). The colonies quantitative results also showed that the number of colonies was significantly reduced after co-transfection ofHSP27andRSK2gene. We indicated that the high expression ofHSP27gene may resist the inflammatory response caused by exogenous stress and enhance the ability of IPEC-J2 to resistE. coliF18 infection.RSK2gene in the MAPK pathway may cooperate withHSP27gene to participate in the immune response of the organism, which provides a theoretical basis for the study of the mechanism of anti-E. coliinfection in piglets.
