Toll 样受体 4 通过促进转录因子 EB 介导的自噬来加重病情。
Toll-Like Receptor 4 Exacerbates via Promoting Transcription Factor EB-Mediated Autophagy.
机构信息
Pediatrics Department, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030014, China.
出版信息
Contrast Media Mol Imaging. 2022 Jul 31;2022:3357694. doi: 10.1155/2022/3357694. eCollection 2022.
() is the most common cause of community-acquired pneumonia. Toll-like receptors (TLRs) play an essential role in pneumonia. The purpose of this study was to investigate the roles of TLR4 in . Mice were administrated with 100 l (1 × 107 ccu/ml) of . HE staining was applied for histological analysis. The protein expression was determined by western blot. The cytokine level was detected by ELISA. The results showed that TLR4-deficient mice were protected from . However, downregulation of TLR4 inhibited inflammatory response and autophagy. Moreover, transcription factor EB (TFEB) participated in -induced inflammatory response and autophagy, while knockdown of TLR4 downregulated TFEB and its nuclear translocation.
（）是社区获得性肺炎的最常见病因。Toll 样受体（TLR）在肺炎中起着至关重要的作用。本研究旨在探讨 TLR4 在 中的作用。用 100μl（1×107 ccu/ml） 处理小鼠。进行 HE 染色进行组织学分析。通过 Western blot 确定蛋白表达。通过 ELISA 检测细胞因子水平。结果表明，TLR4 缺陷型小鼠对 有保护作用。然而，TLR4 的下调抑制了炎症反应和自噬。此外，转录因子 EB（TFEB）参与了 诱导的炎症反应和自噬，而 TLR4 的敲低则下调了 TFEB 及其核转位。
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