• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

糖皮质激素抑制鼻旁窦上皮细胞中 LPS 和 PGN 诱导的 NF-κB 激活。

Glucocorticoids suppress NF-kappaB activation induced by LPS and PGN in paranasal sinus epithelial cells.

机构信息

Department of Otorhinolaryngology and Head and Neck Surgery, Division of Clinical Medical Science, Programs for Applied Biomedicine, Graduate School of Biomedical Science, Hiroshima University, Minami-ku, Hiroshima, Japan.

出版信息

Rhinology. 2009 Dec;47(4):413-8. doi: 10.4193/Rhin08.074.

DOI:10.4193/Rhin08.074
PMID:19936369
Abstract

OBJECTIVES

The aim of this study was to examine the innate immune response induced by toll-like receptors (TLRs) in the paranasal sinus epithelial cells in cell culture models and to examine the effect of glucocorticoids (GCs) on the innate immune response.

METHODS

After stimulation with lipopolysaccharide (LPS) and peptidoglycan (PGN), p50 level was measured as an index of the innate response in the paranasal sinus epithelium. To observe the effect of GCs, the specimens were pre-treated with dexamethasone (DEX) for 48 hours prior to stimulation. On immunocytochemistry GR, TLR2 and TLR4 in the paranasal sinus epithelium were observed.

RESULTS

The p50 activity levels increased after stimulation with LPS and PGN in a dose-dependent manner. Pretreatment with DEX significantly suppressed the increase in p50 activity levels induced by LPS and PGN. On immunocytochemistry, TLR2 and TLR4 immunoreactivities were relatively high after 48h DEX pretreatment.

CONCLUSION

The increase in NF-kappaB activity after LPS and PGN stimulation suggests that stimulation through TLR2 and TLR4 may induce high cytokine expression and inflammatory cell migration in the paranasal sinus epithelial cells. In paranasal sinus epithelial cells GCs not only have anti-inflammatory effects through transcription factor inhibition but also enhance innate host defences.

摘要

目的

本研究旨在探讨细胞培养模型中鼻旁窦上皮细胞 Toll 样受体(TLR)诱导的固有免疫反应,并研究糖皮质激素(GCs)对固有免疫反应的影响。

方法

用脂多糖(LPS)和肽聚糖(PGN)刺激后,以 p50 水平作为鼻旁窦上皮固有反应的指标。为了观察 GCs 的作用,在刺激前用地塞米松(DEX)预处理标本 48 小时。用免疫细胞化学法观察鼻旁窦上皮中的 GR、TLR2 和 TLR4。

结果

LPS 和 PGN 刺激后,p50 活性水平呈剂量依赖性增加。DEX 预处理显著抑制了 LPS 和 PGN 诱导的 p50 活性水平的增加。免疫细胞化学染色显示,DEX 预处理 48 小时后 TLR2 和 TLR4 免疫反应性相对较高。

结论

LPS 和 PGN 刺激后 NF-κB 活性的增加表明,TLR2 和 TLR4 的刺激可能导致鼻旁窦上皮细胞中细胞因子表达和炎症细胞迁移增加。在鼻旁窦上皮细胞中,GCs 不仅通过转录因子抑制具有抗炎作用,而且还增强固有宿主防御。

相似文献

1
Glucocorticoids suppress NF-kappaB activation induced by LPS and PGN in paranasal sinus epithelial cells.糖皮质激素抑制鼻旁窦上皮细胞中 LPS 和 PGN 诱导的 NF-κB 激活。
Rhinology. 2009 Dec;47(4):413-8. doi: 10.4193/Rhin08.074.
2
Upregulation of toll-like receptor 2 gene expression in macrophage response to peptidoglycan and high concentration of lipopolysaccharide is involved in NF-kappa b activation.巨噬细胞对肽聚糖和高浓度脂多糖反应中Toll样受体2基因表达的上调参与核因子κB的激活。
Infect Immun. 2001 May;69(5):2788-96. doi: 10.1128/IAI.69.5.2788-2796.2001.
3
Human intrahepatic biliary epithelial cells function in innate immunity by producing IL-6 and IL-8 via the TLR4-NF-kappaB and -MAPK signaling pathways.人肝内胆管上皮细胞通过TLR4-NF-κB和-MAPK信号通路产生IL-6和IL-8,在固有免疫中发挥作用。
Liver Int. 2006 May;26(4):467-76. doi: 10.1111/j.1478-3231.2006.01254.x.
4
Toll-like receptor 2 and 4 combination engagement upregulate IL-15 synergistically in human rheumatoid synovial fibroblasts.Toll样受体2和4联合激活可协同上调人类风湿性滑膜成纤维细胞中的白细胞介素-15。
Immunol Lett. 2007 Mar 15;109(1):21-7. doi: 10.1016/j.imlet.2006.12.006. Epub 2007 Jan 17.
5
Toll-like receptor 4 initiates an innate immune response to lipopolysaccharide in human conjunctival epithelial cells.Toll样受体4在人结膜上皮细胞中引发对脂多糖的先天性免疫反应。
Exp Eye Res. 2009 Jan;88(1):49-56. doi: 10.1016/j.exer.2008.09.017. Epub 2008 Oct 9.
6
Triggering of toll-like receptors 2 and 4 by Aspergillus fumigatus conidia in immortalized human corneal epithelial cells to induce inflammatory cytokines.烟曲霉分生孢子触发永生化人角膜上皮细胞中的Toll样受体2和4以诱导炎性细胞因子。
Chin Med J (Engl). 2008 Mar 5;121(5):450-4.
7
Dialyzable leukocyte extract differentially regulates the production of TNFalpha, IL-6, and IL-8 in bacterial component-activated leukocytes and endothelial cells.可透析白细胞提取物对细菌成分激活的白细胞和内皮细胞中肿瘤坏死因子α、白细胞介素-6和白细胞介素-8的产生具有不同的调节作用。
Inflamm Res. 2005 Feb;54(2):74-81. doi: 10.1007/s00011-004-1326-5.
8
Toll-like receptor (TLR) 2 induced through TLR4 signaling initiated by Helicobacter pylori cooperatively amplifies iNOS induction in gastric epithelial cells.由幽门螺杆菌引发的Toll样受体4(TLR4)信号传导所诱导的Toll样受体2(TLR2),协同增强胃上皮细胞中诱导型一氧化氮合酶(iNOS)的诱导作用。
Am J Physiol Gastrointest Liver Physiol. 2007 Nov;293(5):G1004-12. doi: 10.1152/ajpgi.00096.2007. Epub 2007 Sep 13.
9
Prostate epithelial cells can act as early sensors of infection by up-regulating TLR4 expression and proinflammatory mediators upon LPS stimulation.前列腺上皮细胞可通过在脂多糖刺激下上调Toll样受体4(TLR4)的表达和促炎介质,充当感染的早期传感器。
J Leukoc Biol. 2006 May;79(5):989-98. doi: 10.1189/jlb.1005597. Epub 2006 Mar 7.
10
Toll-like receptor 2 and 4 expression after severe injury is not involved in the dysregulation of the innate immune system.严重损伤后Toll样受体2和4的表达与先天免疫系统的失调无关。
J Trauma. 2007 Oct;63(4):740-6. doi: 10.1097/01.ta.0000240451.42238.d1.

引用本文的文献

1
TLR Signals in Epithelial Cells in the Nasal Cavity and Paranasal Sinuses.鼻腔和鼻窦上皮细胞中的Toll样受体信号
Front Allergy. 2021 Nov 22;2:780425. doi: 10.3389/falgy.2021.780425. eCollection 2021.
2
The Functional Diversity of Nitric Oxide Synthase Isoforms in Human Nose and Paranasal Sinuses: Contrasting Pathophysiological Aspects in Nasal Allergy and Chronic Rhinosinusitis.一氧化氮合酶同工型在人鼻腔和副鼻窦中的功能多样性:变应性鼻炎和慢性鼻-鼻窦炎的对比病理生理学方面。
Int J Mol Sci. 2021 Jul 15;22(14):7561. doi: 10.3390/ijms22147561.
3
Non-Reflex Defense Mechanisms of Upper Airway Mucosa: Possible Clinical Application.
上呼吸道黏膜的非反射防御机制:可能的临床应用。
Physiol Res. 2020 Mar 27;69(Suppl 1):S55-S67. doi: 10.33549/physiolres.934404.
4
Regulation of KDM2B and Brg1 on Inflammatory Response of Nasal Mucosa in CRSwNP.KDM2B 和 Brg1 对 CRSwNP 鼻黏膜炎症反应的调控。
Inflammation. 2019 Aug;42(4):1389-1400. doi: 10.1007/s10753-019-01000-6.
5
ICON: chronic rhinosinusitis.慢性鼻-鼻窦炎
World Allergy Organ J. 2014 Oct 27;7(1):25. doi: 10.1186/1939-4551-7-25. eCollection 2014.
6
The role of TNF-α in inflammatory olfactory loss.肿瘤坏死因子-α在炎症性嗅觉丧失中的作用。
Laryngoscope. 2011 Nov;121(11):2481-6. doi: 10.1002/lary.22190. Epub 2011 Aug 31.