spd1672, a novel in vivo-induced gene, affects inflammatory response in a murine model of Streptococcus pneumoniae infection
spd1672, a novel in vivo-induced gene, affects inflammatory response in a murine model of Streptococcus pneumoniae infection
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spd1672 是一种新型体内诱导基因，可影响肺炎链球菌感染小鼠模型的炎症反应
DOI：
10.1139/cjm-2017-0662
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发表时间：
2018
影响因子：
2.8
通讯作者：
Wang Hong
中科院分区：
文献类型：
--
作者：
Gan Lingling;Zhang Xuemei;Xu Xiuyu;Xu Wenchun;Lu Chang;Cui Jin;Wang Hong
spd 1672是一种新的肺炎链球菌（Streptococcus pneumoniae，S. pn）基因在体内被诱导表达，该基因与S.然而，spd 1672在宿主针对S.感染情况不明。在本研究中，小鼠感染野生型D39和突变型D39Δ spd 1672株。与D39感染的小鼠相比，在D39Δ spd 1672处理的小鼠中观察到细菌负荷减少和炎症反应减弱。D39Δ spd 1672感染组小鼠血液中促炎细胞因子IFN-γ、TNF-α和IL-1β水平低于D39感染组。此外，在D39Δ spd 1672感染的小鼠中观察到STAT 3和AKT活化减弱。总之，我们的数据表明，spd 1672表达调节促炎细胞因子的释放，AKT-STAT 3信号似乎参与了这一过程。总之，本研究扩展了我们对体内诱导基因在S.pn-宿主相互作用中的作用的理解。
spd1672, a novelStreptococcus pneumoniae(hereinafterS. pn) gene induced in vivo, has been identified to contribute to the virulence ofS. pn; however, the role ofspd1672during host innate immune reaction againstS. pninfection is unknown. In the present study, mice were infected with wild-type D39 and mutant D39Δspd1672strains. Compared with the D39-infected mice, reduced bacterial load and attenuated inflammatory response were observed in the D39Δspd1672-treated mice. The levels of proinflammatory cytokines, including IFN-γ, TNF-α, and IL-1β, in the blood of D39Δspd1672-infected mice were lower than that in the D39-infected group. Additionally, attenuated activation of STAT3 and AKT was observed in the D39Δspd1672-infected mice. In conclusion, our data indicated thatspd1672expression modulates the release of proinflammatory cytokines, and AKT–STAT3 signaling appears to participate in the process. In conclusion, the present study extends our understanding of the role of an in vivo-induced gene inS. pn–host interaction.