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TGFβ depletion does neither modulate acute E. coli-induced inflammatory immune responses nor impair the protective effect by chronic filarial infection

机译:TGFβ耗竭既不调节急性大肠杆菌诱导的炎症免疫反应也不损害慢性丝虫感染的保护作用

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摘要

TGFβ is an anti-inflammatory molecule that suppresses pro-inflammatory immune responses. Previously, we demonstrated that chronic filarial infection has a beneficial impact on -induced sepsis. In the present study, we investigated whether this protective effect is dependent on TGFβ signaling and whether depletion of TGFβ before challenge alters the early course of sepsis . depletion of TGFβ before challenge did not alter levels of pro-inflammatory cytokines/chemokines and did neither increase the bacterial burden nor worsen -induced hypothermia six hours post challenge. Similarly, in the co-infection model, despite TGFβ depletion, mice infected with the filarial nematode exhibited milder -induced hypothermia, reduced bacterial load and pro-inflammatory immune responses. Thus, we conclude that TGFβ is not essentially modulating the initial pro-inflammatory phase during sepsis and that the protective effect of a chronic filarial infection against sepsis is independent of TGFβ signaling.
机译:TGFβ是一种抑制炎性免疫反应的抗炎分子。以前,我们证明了慢性丝虫感染对诱发败血症具有有益的影响。在本研究中,我们研究了这种保护作用是否取决于TGFβ信号传导,以及攻击前TGFβ的消耗是否会改变败血症的早期过程。攻击前6小时TGFβ的消耗并没有改变促炎细胞因子/趋化因子的水平,并且在攻击后6小时既没有增加细菌负担也没有加重诱导的体温过低。同样,在共感染模型中,尽管TGFβ耗竭,但感染了丝虫线虫的小鼠 表现出较温和的诱导体温过低,细菌负荷降低和促炎性免疫反应。因此,我们得出的结论是,TGFβ在败血症过程中基本上不调节初始促炎期,并且慢性丝状感染对败血症的保护作用独立于TGFβ信号传导。

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