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Heat stress upregulation of Toll-like receptors 2/4 and acute inflammatory cytokines in peripheral blood mononuclear cell (PBMC) of Bama miniature pigs: an in vivo and in vitro study  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Heat stress upregulation of Toll-like receptors 2/4 and acute inflammatory cytokines in peripheral blood mononuclear cell (PBMC) of Bama miniature pigs: an in vivo and in vitro study

作者:Ju, X. -H.[1,2];Xu, H. -J.[3];Yong, Y. -H.[1];An, L. -L.[3];Jiao, P. -R.[2];Liao, M.[2]

机构:[1]Guangdong Ocean Univ, Dept Vet Med, Zhanjiang 524088, Peoples R China;[2]South China Agr Univ, Coll Vet Med, Key Lab Zoonoses Control & Prevent Guangdong, MOA Key Lab Anim Vaccine Dev, Guangzhou 510642, Guangdong, Peoples R China;[3]Guangdong Ocean Univ, Dept Anim Sci, Zhanjiang 524088, Peoples R China

年份:2014

卷号:8

期号:9

起止页码:1462

外文期刊名:ANIMAL

收录:SCI-EXPANDED(收录号:WOS:000342219000010)、、Scopus(收录号:2-s2.0-84906311527)、WOS

基金:This research was supported by grants from the National Natural Science Foundation of China (No. 31101862), grants from China Postdoctor Science Foundation and Guangdong Ocean University Doctor Seed Grant (No. 0712107).

语种:英文

外文关键词:Bama miniature pig; heat stress; inflammatory cytokine; Toll-like receptors

外文摘要:Global warming is a challenge to animal health, because of increased heat stress, with subsequent induction of immunosuppression and increased susceptibility to disease. Toll-like receptors (TLR) are pattern recognition receptors that act as sentinels of pathogen invasion and tissue damage. Ligation of TLRs results in a signaling cascade and production of inflammatory cytokines, which eradicate pathogens and maintain the health of the host. We hypothesized that the TLR signaling pathway plays a role in immunosuppression in heat-stressed pigs. We explored the changes in the expression of TLR2, TLR4 and the concentration of acute inflammatory cytokines, such as IL-2, IL-8, IL-12 and IFN-gamma in Bama miniature pigs subjected to 21 consecutive days of heat stress, both in vitro and in vivo models. The results showed that heat stress induced the upregulation of cortisol in the plasma of pigs (P < 0.05); TLR4 mRNA was elevated, but IL-2 was reduced in peripheral blood mononuclear cells (PBMC, P < 0.05). The white blood cell count and the percentage of granulocytes (eosinophilic + basophilic) decreased significantly in heat-stressed pigs (P < 0.05). In the in vitro model (PBMC heat shocked for 1 h followed by a 9 h recovery period), TLR2 and TLR4 mRNA expression also increased, as did the concentration of IL-12 in supernatants. However, IFN-gamma was significantly reduced in PBMC culture supernatants (P < 0.05). We concluded that a consecutive heat stress period elevated the expression of TLR2 and TLR4 in PBMC and increased the plasma levels of inflammatory cytokines. These data indicate that TLR activation and dysregulation of cytokine expression in response to prolonged heat stress may be associated with immunosuppression and increased susceptibility to antigenic challenge in Bama miniature pigs.

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