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Type I interferon signalling is not required for the induction of endotoxin tolerance

机译：I型干扰素信号不需要诱导内毒素耐受性

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摘要

Endotoxin, or LPS tolerance, is an immunomodulatory mechanism that results in a significantly diminished response to secondary LPS exposure, which may serve to protect the host against endotoxic shock. Type I interferons (IFNs) are cytokines released upon LPS binding to TLR4 and have been shown to have immunomodulatory properties. Due to this regulatory function of type I IFN, we aimed to investigate the role of type I IFN signalling in LPS tolerance. Our data suggests that type I IFN does not play a role in LPS tolerance in vitro, as both wild type and IFNAR1(-/-) peritoneal macrophages showed reduced cytokine production after secondary LPS exposure. Furthermore, both wild type and IFNAR1(-/-) mice were protected from a lethal dose of LPS after receiving three small doses to induce tolerance. However, IFNAR(-/-)-Imice seemed to recover faster than wild type mice, suggesting type I IFN signalling plays a detrimental role in LPS-induced sepsis. Although type I IFN may have a regulatory function in microbial infections, it does not seem to play a role in endotoxin tolerance. Type I IFN involvement in bacterial infection remains complex and further studies are needed to define the regulatory function of type I IFN signalling. (C) 2017 Elsevier Ltd. All rights reserved.
机译：内毒素或LPS耐受性是一种免疫调节机制，导致对次级LPS暴露的响应显着减少，这可能用于保护宿主免受内毒休克。 I型干扰素（IFNS）是在LPS结合到TLR4时释放的细胞因子，并且已被证明具有免疫调节性质。由于I IFN类型的调节功能，我们旨在调查I IFN信号传导在LPS公差中的作用。我们的数据表明，I型IFN在体外不发挥LPS耐受性的作用，因为野生型和IFNAR1（ - / - ）腹膜巨噬细胞显示出次级LPS暴露后的细胞因子产生降低。此外，在接受三个小剂量以诱导耐受后，保护野生型和IFNAR1（ - / - ）小鼠免受致死剂量的LPS。然而，IFNAR（ - / - ） - 似似乎比野生型小鼠恢复得更快，建议I IFN信号传导在LPS诱导的败血症中起着不利作用。虽然I IFN IFN可能在微生物感染中具有调节功能，但似乎在内毒素耐受性中似乎并不起作用。 I型IFN参与细菌感染仍然复杂，需要进一步的研究来定义I型IFN信号传导的调节功能。 （c）2017 Elsevier Ltd.保留所有权利。

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