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幽门螺杆菌感染通过 Toll 样受体 8 信号诱导人单核细胞产生 I 型干扰素反应。

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling.

机构信息

Department of Medical Microbiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.

School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC 3083, Australia.

出版信息

J Immunol Res. 2022 Oct 22;2022:3861518. doi: 10.1155/2022/3861518. eCollection 2022.

DOI:10.1155/2022/3861518
PMID:36317079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9617731/
Abstract

colonization and persistence could precede gastric adenocarcinoma. Elucidating immune recognition strategies of is therefore imperative to curb chronic persistence in the human host. Toll-like receptor 7 (TLR7) and TLR8 are widely known as viral single-stranded RNA (ssRNA) sensors yet less studied in the bacteria context. Here, we investigated the involvement of these receptors in the immunity to . Human THP-1 monocytic cells were infected with , and the expression levels of human Toll-like receptors (TLRs) were examined. The roles of TLR7 and TLR8 in response to infection were further investigated using receptor antagonists. Among all TLR transcripts examined, TLR8 exhibited the most prominent upregulation, followed by TLR7 in the THP-1 cells infected with J99 or SS1 strains. infection-mediated IFN- and IFN- transactivation was significantly abrogated by the TLR7/8 (but not TLR7) antagonist. Additionally, TLR7/8 antagonist treatment reduced infection-mediated phosphorylation of interferon regulatory factor 7 (IRF7). Our study suggests a novel role of TLR8 signaling in host immunity against through sensing live bacteria to elicit the production of type I interferon.

摘要

定植和持续存在可能先于胃腺癌。因此,阐明宿主中对 慢性持续存在的免疫识别策略对于遏制其发展至关重要。Toll 样受体 7(TLR7)和 TLR8 是众所周知的病毒单链 RNA(ssRNA)传感器,但在细菌环境中的研究较少。在这里,我们研究了这些受体在对 的免疫中的参与。用 感染人 THP-1 单核细胞,并检查人 Toll 样受体(TLR)的表达水平。使用受体拮抗剂进一步研究了 TLR7 和 TLR8 在对 感染的反应中的作用。在所检查的所有 TLR 转录本中,TLR8 的上调最为明显,其次是在感染 J99 或 SS1 株的 THP-1 细胞中 TLR7。TLR7/8(而非 TLR7)拮抗剂显著阻断了 感染介导的 IFN-和 IFN-的反式激活。此外,TLR7/8 拮抗剂处理降低了 感染介导的干扰素调节因子 7(IRF7)的磷酸化。我们的研究表明 TLR8 信号在宿主对 通过感知活菌来产生 I 型干扰素的免疫中发挥了新的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/c03c20f3f3a5/JIR2022-3861518.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/0d7255335f14/JIR2022-3861518.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/b8fd22dc2965/JIR2022-3861518.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/f5c8a6a12f50/JIR2022-3861518.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/d23d7a9ef285/JIR2022-3861518.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/bf713ce2aaed/JIR2022-3861518.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/05d902272c60/JIR2022-3861518.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/47345d7b33e4/JIR2022-3861518.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/0453fed937a0/JIR2022-3861518.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/c03c20f3f3a5/JIR2022-3861518.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/0d7255335f14/JIR2022-3861518.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/b8fd22dc2965/JIR2022-3861518.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/f5c8a6a12f50/JIR2022-3861518.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/d23d7a9ef285/JIR2022-3861518.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/bf713ce2aaed/JIR2022-3861518.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/05d902272c60/JIR2022-3861518.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/47345d7b33e4/JIR2022-3861518.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/0453fed937a0/JIR2022-3861518.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9e5/9617731/c03c20f3f3a5/JIR2022-3861518.009.jpg

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