• 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

铜绿假单胞菌和缓症链球菌混合感染对急性肺炎小鼠模型中TLR4介导的免疫反应的影响

Effects of Pseudomonas aeruginosa and Streptococcus mitis mixed infection on TLR4-mediated immune response in acute pneumonia mouse model.

作者信息

Song Chao, Li Hongdong, Zhang Yunhui, Yu Jialin

机构信息

Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China.

Ministry of Education Key Laboratory of Child Development and Disorders - Chongqing Key Laboratory of Pediatrics, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, China.

出版信息

BMC Microbiol. 2017 Apr 4;17(1):82. doi: 10.1186/s12866-017-0999-1.

DOI:10.1186/s12866-017-0999-1
PMID:28376744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5381141/
Abstract

BACKGROUND

Our previous research on the diversity of microbiota in the endotracheal tubes (ETTs) of neonates in the neonatal intensive care unit found that Pseudomonas aeruginosa (P. aeruginosa) and Streptococcus mitis (S. mitis) were the dominant bacteria on the ETT surface and the existence of S. mitis could promote biofilm formation and pathogenicity of P. aeruginosa. Toll-like receptor 4 (TLR4), which has been widely detected on the surface of airway epithelial cells, is the important component of the innate immune system. Therefore, we hypothesized that the co-existence of these two bacteria might impact the host immune system through TLR4 signaling.

RESULTS

S. mitis rarely caused inflammation, whereas P. aeruginosa caused the most severe inflammation accompanied by increases in the number of inflammatory cells, interleukin (IL)-6 and tumor necrosis factor (TNF)-α expression, and total cell counts in BALF (p < 0.05). In the PAO1 + S. mitis group, moderate inflammation, reduced IL-6 and TNF-α protein levels, and decreased total cell counts were observed. Additionally, levels of these indicators were decreased lower in TLR4-deficient mice than in wild-type mice (p < 0.05).

CONCLUSIONS

Our results demonstrated that infection with S. mitis together with P. aeruginosa could alleviate lung inflammation in acute lung infection mouse models possibly via the TLR4 signaling pathway.

摘要

背景

我们之前对新生儿重症监护病房新生儿气管内插管(ETT)中微生物群多样性的研究发现,铜绿假单胞菌(P. aeruginosa)和缓症链球菌(S. mitis)是ETT表面的主要细菌,且缓症链球菌的存在可促进铜绿假单胞菌生物膜的形成和致病性。Toll样受体4(TLR4)在气道上皮细胞表面广泛表达,是固有免疫系统的重要组成部分。因此,我们推测这两种细菌的共存可能通过TLR4信号通路影响宿主免疫系统。

结果

缓症链球菌很少引起炎症,而铜绿假单胞菌引起最严重的炎症,伴有炎性细胞数量增加、白细胞介素(IL)-6和肿瘤坏死因子(TNF)-α表达增加以及支气管肺泡灌洗液(BALF)中总细胞计数增加(p < 0.05)。在PAO1 + 缓症链球菌组中,观察到中度炎症、IL-6和TNF-α蛋白水平降低以及总细胞计数减少。此外,这些指标在TLR4缺陷小鼠中的降低程度低于野生型小鼠(p < 0.05)。

结论

我们的结果表明,在急性肺部感染小鼠模型中,缓症链球菌与铜绿假单胞菌共同感染可能通过TLR4信号通路减轻肺部炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/d566866bda76/12866_2017_999_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/bdef4b8300f6/12866_2017_999_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/0d931251adf0/12866_2017_999_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/6635ac5b1043/12866_2017_999_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/d566866bda76/12866_2017_999_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/bdef4b8300f6/12866_2017_999_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/0d931251adf0/12866_2017_999_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/6635ac5b1043/12866_2017_999_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37e8/5381141/d566866bda76/12866_2017_999_Fig4_HTML.jpg

相似文献

1
Effects of Pseudomonas aeruginosa and Streptococcus mitis mixed infection on TLR4-mediated immune response in acute pneumonia mouse model.铜绿假单胞菌和缓症链球菌混合感染对急性肺炎小鼠模型中TLR4介导的免疫反应的影响
BMC Microbiol. 2017 Apr 4;17(1):82. doi: 10.1186/s12866-017-0999-1.
2
Does Streptococcus mitis, a neonatal oropharyngeal bacterium, influence the pathogenicity of Pseudomonas aeruginosa?新生儿口咽细菌缓症链球菌会影响铜绿假单胞菌的致病性吗?
Microbes Infect. 2015 Oct;17(10):710-6. doi: 10.1016/j.micinf.2015.08.001. Epub 2015 Aug 13.
3
TNF-alpha decreases infection-induced lung injury in burn through negative regulation of TLR4/iNOS.肿瘤坏死因子-α通过负调控 TLR4/iNOS 减少烧伤感染引起的肺损伤。
J Surg Res. 2013 Jan;179(1):106-14. doi: 10.1016/j.jss.2012.08.038. Epub 2012 Sep 7.
4
TLR4-interacting SPA4 peptide improves host defense and alleviates tissue injury in a mouse model of Pseudomonas aeruginosa lung infection.TLR4 相互作用的 SPA4 肽可改善铜绿假单胞菌肺部感染小鼠模型的宿主防御并减轻组织损伤。
PLoS One. 2019 Jan 28;14(1):e0210979. doi: 10.1371/journal.pone.0210979. eCollection 2019.
5
Streptococcus pneumoniae Endopeptidase O (PepO) Elicits a Strong Innate Immune Response in Mice via TLR2 and TLR4 Signaling Pathways.肺炎链球菌内肽酶O(PepO)通过TLR2和TLR4信号通路在小鼠中引发强烈的先天性免疫反应。
Front Cell Infect Microbiol. 2016 Feb 29;6:23. doi: 10.3389/fcimb.2016.00023. eCollection 2016.
6
Toll-like receptor 2 represses nonpilus adhesin-induced signaling in acute infections with the Pseudomonas aeruginosa pilA mutant.Toll样受体2抑制铜绿假单胞菌pilA突变体急性感染中非菌毛黏附素诱导的信号传导。
Infect Immun. 2004 Aug;72(8):4561-9. doi: 10.1128/IAI.72.8.4561-4569.2004.
7
Protease IV Exacerbates Pneumococcal Pneumonia and Systemic Disease.蛋白酶 IV 加剧肺炎链球菌性肺炎及全身疾病。
mSphere. 2018 May 2;3(3). doi: 10.1128/mSphere.00212-18. eCollection 2018 May-Jun.
8
Pseudomonas aeruginosa outer membrane vesicles modulate host immune responses by targeting the Toll-like receptor 4 signaling pathway.铜绿假单胞菌外膜囊泡通过靶向 Toll 样受体 4 信号通路调节宿主免疫反应。
Infect Immun. 2013 Dec;81(12):4509-18. doi: 10.1128/IAI.01008-13. Epub 2013 Sep 30.
9
Toll-like receptor 9 deficiency protects mice against Pseudomonas aeruginosa lung infection.Toll样受体9缺陷可保护小鼠免受铜绿假单胞菌肺部感染。
PLoS One. 2014 Mar 4;9(3):e90466. doi: 10.1371/journal.pone.0090466. eCollection 2014.
10
Autoinducer-2 of Streptococcus mitis as a Target Molecule to Inhibit Pathogenic Multi-Species Biofilm Formation In Vitro and in an Endotracheal Intubation Rat Model.缓症链球菌的自诱导物-2作为一种靶分子在体外和气管插管大鼠模型中抑制致病性多物种生物膜形成
Front Microbiol. 2016 Feb 8;7:88. doi: 10.3389/fmicb.2016.00088. eCollection 2016.

引用本文的文献

1
Reply to David et al, "Studying pathogenesis: the need for more than just the PAO1 strain".对大卫等人《研究发病机制:不仅仅需要PAO1菌株》一文的回复
Microbiol Spectr. 2025 Sep 2;13(9):e0117725. doi: 10.1128/spectrum.01177-25. Epub 2025 Aug 11.
2
-Induced NLRP3 Inflammasome Activation and Its Downstream Interleukin-1β Release Depend on Caspase-4.诱导的NLRP3炎性小体激活及其下游白细胞介素-1β释放依赖于半胱天冬酶-4。
Front Microbiol. 2020 Aug 13;11:1881. doi: 10.3389/fmicb.2020.01881. eCollection 2020.
3
Differential influence of Streptococcus mitis on host response to metals in reconstructed human skin and oral mucosa.

本文引用的文献

1
Device-associated infections in the pediatric intensive care unit at the American University of Beirut Medical Center.贝鲁特美国大学医疗中心儿科重症监护病房中的设备相关感染
J Infect Dev Ctries. 2016 Jun 30;10(6):554-62. doi: 10.3855/jidc.7303.
2
Imidacloprid induced histomorphological changes and expression of TLR-4 and TNFα in lung.吡虫啉诱导肺组织的组织形态学变化以及Toll样受体4(TLR-4)和肿瘤坏死因子α(TNFα)的表达。
Pestic Biochem Physiol. 2016 Jul;131:9-17. doi: 10.1016/j.pestbp.2016.02.004. Epub 2016 Feb 24.
3
Autoinducer-2 of Streptococcus mitis as a Target Molecule to Inhibit Pathogenic Multi-Species Biofilm Formation In Vitro and in an Endotracheal Intubation Rat Model.
变形链球菌对重建人体皮肤和口腔黏膜中金属宿主反应的差异影响。
Contact Dermatitis. 2020 Nov;83(5):347-360. doi: 10.1111/cod.13668. Epub 2020 Aug 31.
4
Small Molecule Inhibitor of Type Three Secretion System Belonging to a Class 2,4-disubstituted-4H-[1,3,4]-thiadiazine-5-ones Improves Survival and Decreases Bacterial Loads in an Airway Infection in Mice.属于 2,4-二取代-4H-[1,3,4]-噻二嗪-5-酮类的 III 型分泌系统小分子抑制剂可改善气道感染小鼠的存活率并降低细菌载量。
Biomed Res Int. 2018 Sep 10;2018:5810767. doi: 10.1155/2018/5810767. eCollection 2018.
5
Dysbiosis of the Urinary Microbiota Associated With Urine Levels of Proinflammatory Chemokine Interleukin-8 in Female Type 2 Diabetic Patients.2型糖尿病女性患者尿液微生物群失调与促炎趋化因子白细胞介素-8尿液水平的关系
Front Immunol. 2017 Aug 25;8:1032. doi: 10.3389/fimmu.2017.01032. eCollection 2017.
6
Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity.共生菌群维持肺泡巨噬细胞低水平 CCL24 产生以产生抗肿瘤转移活性。
Sci Rep. 2017 Aug 7;7(1):7471. doi: 10.1038/s41598-017-08264-8.
缓症链球菌的自诱导物-2作为一种靶分子在体外和气管插管大鼠模型中抑制致病性多物种生物膜形成
Front Microbiol. 2016 Feb 8;7:88. doi: 10.3389/fmicb.2016.00088. eCollection 2016.
4
LPS- or Pseudomonas aeruginosa-mediated activation of the macrophage TLR4 signaling cascade depends on membrane lipid composition.脂多糖或铜绿假单胞菌介导的巨噬细胞Toll样受体4信号级联反应的激活取决于膜脂质组成。
PeerJ. 2016 Feb 4;4:e1663. doi: 10.7717/peerj.1663. eCollection 2016.
5
Zinc oxide and titanium dioxide nanoparticles induce oxidative stress, inhibit growth, and attenuate biofilm formation activity of Streptococcus mitis.氧化锌和二氧化钛纳米颗粒可诱导氧化应激、抑制生长并减弱缓症链球菌的生物膜形成活性。
J Biol Inorg Chem. 2016 Jun;21(3):295-303. doi: 10.1007/s00775-016-1339-x. Epub 2016 Feb 2.
6
Sensing Gram-negative bacteria: a phylogenetic perspective.感知革兰氏阴性菌:系统发育视角
Curr Opin Immunol. 2016 Feb;38:8-17. doi: 10.1016/j.coi.2015.10.007. Epub 2015 Nov 12.
7
Molecular analysis of biofilms on the surface of neonatal endotracheal tubes based on 16S rRNA PCR-DGGE and species-specific PCR.基于16S rRNA PCR-DGGE和种属特异性PCR的新生儿气管内导管表面生物膜的分子分析
Int J Clin Exp Med. 2015 Jul 15;8(7):11075-84. eCollection 2015.
8
IL-6 as a keystone cytokine in health and disease.IL-6 作为健康与疾病中的关键细胞因子。
Nat Immunol. 2015 May;16(5):448-57. doi: 10.1038/ni.3153.
9
Impact of fish oils on the outcomes of a mouse model of acute Pseudomonas aeruginosa pulmonary infection.鱼油对铜绿假单胞菌急性肺部感染小鼠模型结果的影响。
Br J Nutr. 2015 Jan 28;113(2):191-9. doi: 10.1017/S0007114514003705. Epub 2015 Jan 7.
10
Regulatory T cell activity is partly inhibited in a mouse model of chronic Pseudomonas aeruginosa lung infection.在慢性铜绿假单胞菌肺部感染的小鼠模型中,调节性T细胞的活性受到部分抑制。
Exp Lung Res. 2015 Feb;41(1):44-55. doi: 10.3109/01902148.2014.964351. Epub 2014 Nov 14.