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食源性病原体低酰化 LPS 诱导小鼠巨噬细胞中 TLR4 介导的适度炎症反应。

Hypoacylated LPS from Foodborne Pathogen Induces Moderate TLR4-Mediated Inflammatory Response in Murine Macrophages.

机构信息

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.

Department of Immunology, Biological Faculty, Lomonosov Moscow State University, Moscow, Russia.

出版信息

Front Cell Infect Microbiol. 2018 Feb 27;8:58. doi: 10.3389/fcimb.2018.00058. eCollection 2018.

DOI:10.3389/fcimb.2018.00058
PMID:29535976
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5835049/
Abstract

Toll-like receptor 4 (TLR4) initiates immune response against Gram-negative bacteria upon specific recognition of lipid A moiety of lipopolysaccharide (LPS), the major component of their cell wall. Some natural differences between LPS variants in their ability to interact with TLR4 may lead to either insufficient activation that may not prevent bacterial growth, or excessive activation which may lead to septic shock. In this study we evaluated the biological activity of LPS isolated from pathogenic strain of , the most widespread bacterial cause of foodborne diarrhea in humans. With the help of hydrophobic chromatography and MALDI-TOF mass spectrometry we showed that LPS from a strain O2A consists of both hexaacyl and tetraacyl forms. Since such hypoacylation can result in a reduced immune response in humans, we assessed the activity of LPS from in mouse macrophages by measuring its capacity to activate TLR4-mediated proinflammatory cytokine and chemokine production, as well as NFκB-dependent reporter gene transcription. Our data support the hypothesis that LPS acylation correlates with its bioactivity.

摘要

Toll 样受体 4（TLR4）在特异性识别脂多糖（LPS）的脂质 A 部分后，启动针对革兰氏阴性细菌的免疫反应，LPS 是其细胞壁的主要成分。LPS 变体在与 TLR4 相互作用的能力方面存在一些天然差异，这可能导致激活不足，无法阻止细菌生长，或过度激活，导致感染性休克。在这项研究中，我们评估了从人类食源性腹泻最常见的细菌病原体中分离出的 LPS 的生物学活性。借助疏水层析和 MALDI-TOF 质谱，我们表明 O2A 血清型的 LPS 由六酰基和四酰基形式组成。由于这种低酰化可能导致人类的免疫反应减弱，因此我们通过测量其激活 TLR4 介导的促炎细胞因子和趋化因子产生以及 NFκB 依赖性报告基因转录的能力，评估了来自 菌株的 LPS 的活性。我们的数据支持 LPS 酰化与其生物活性相关的假设。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/6c8ec892a434/fcimb-08-00058-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/0341cd6071e8/fcimb-08-00058-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/c227d461029f/fcimb-08-00058-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/3889c0242662/fcimb-08-00058-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/1bb0e7b014bf/fcimb-08-00058-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/de4639e1eae2/fcimb-08-00058-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/6c8ec892a434/fcimb-08-00058-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/0341cd6071e8/fcimb-08-00058-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/c227d461029f/fcimb-08-00058-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/3889c0242662/fcimb-08-00058-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/1bb0e7b014bf/fcimb-08-00058-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/de4639e1eae2/fcimb-08-00058-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aabc/5835049/6c8ec892a434/fcimb-08-00058-g0006.jpg

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