Suppr超能文献

β-溶血性B组链球菌色素的促血栓形成和促炎活性

Prothrombotic and Proinflammatory Activities of the β-Hemolytic Group B Streptococcal Pigment.

作者信息

Siemens Nikolai, Oehmcke-Hecht Sonja, Hoßmann Jörn, Skorka Sebastian B, Nijhuis Roel H T, Ruppen Corinne, Skrede Steinar, Rohde Manfred, Schultz Daniel, Lalk Michael, Itzek Andreas, Pieper Dietmar H, van den Bout Christiaan J, Claas Eric C J, Kuijper Ed J, Mauritz Robert, Sendi Parham, Wunderink Herman F, Norrby-Teglund Anna

机构信息

Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Huddinge, Sweden,

Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, University of Greifswald, Greifswald, Germany,

出版信息

J Innate Immun. 2020;12(4):291-303. doi: 10.1159/000504002. Epub 2019 Nov 19.

Abstract

A prominent feature of severe streptococcal infections is the profound inflammatory response that contributes to systemic toxicity. In sepsis the dysregulated host response involves both immunological and nonimmunological pathways. Here, we report a fatal case of an immunocompetent healthy female presenting with toxic shock and purpura fulminans caused by group B streptococcus (GBS; serotype III, CC19). The strain (LUMC16) was pigmented and hyperhemolytic. Stimulation of human primary cells with hyperhemolytic LUMC16 and STSS/NF-HH strains and pigment toxin resulted in a release of proinflammatory mediators, including tumor necrosis factor, interleukin (IL)-1β, and IL-6. In addition, LUMC16 induced blood clotting and showed factor XII activity on its surface, which was linked to the presence of the pigment. The expression of pigment was not linked to a mutation within the CovR/S region. In conclusion, our study shows that the hemolytic lipid toxin contributes to the ability of GBS to cause systemic hyperinflammation and interferes with the coagulation system.

摘要

严重链球菌感染的一个显著特征是导致全身毒性的强烈炎症反应。在脓毒症中,失调的宿主反应涉及免疫和非免疫途径。在此,我们报告一例由B族链球菌(GBS;血清型III,CC19)引起的中毒性休克和暴发性紫癜的免疫功能正常健康女性死亡病例。该菌株(LUMC16)有色素沉着且溶血活性增强。用溶血活性增强的LUMC16和STSS/NF-HH菌株以及色素毒素刺激人原代细胞会导致促炎介质的释放,包括肿瘤坏死因子、白细胞介素(IL)-1β和IL-6。此外,LUMC16诱导血液凝固并在其表面显示出因子XII活性,这与色素的存在有关。色素的表达与CovR/S区域内的突变无关。总之,我们的研究表明溶血脂质毒素有助于GBS引起全身过度炎症并干扰凝血系统。

相似文献

1
Prothrombotic and Proinflammatory Activities of the β-Hemolytic Group B Streptococcal Pigment.
J Innate Immun. 2020;12(4):291-303. doi: 10.1159/000504002. Epub 2019 Nov 19.
4
Phenotypic and molecular characterization of hyperpigmented group B Streptococci.
Int J Med Microbiol. 2014 Jul;304(5-6):717-24. doi: 10.1016/j.ijmm.2014.05.003. Epub 2014 May 16.
5
Group B Streptococcal Hemolytic Pigment Impairs Platelet Function in a Two-Step Process.
Cells. 2022 May 13;11(10):1637. doi: 10.3390/cells11101637.
7
Group B Streptococcal Toxic Shock Syndrome and covR/S Mutations Revisited.
Emerg Infect Dis. 2017 Jan;23(1):150-152. doi: 10.3201/eid2301.161063.
8
Group B Streptococcus Induces a Robust IFN-γ Response by CD4(+) T Cells in an In Vitro and In Vivo Model.
J Immunol Res. 2016;2016:5290604. doi: 10.1155/2016/5290604. Epub 2016 Feb 16.
10
Streptococcus agalactiae infection in zebrafish larvae.
Microb Pathog. 2015 Feb;79:57-60. doi: 10.1016/j.micpath.2015.01.007. Epub 2015 Jan 21.

引用本文的文献

1
Single-Molecule Identification of the Isomers of a Lipidic Antibody Activator.
J Phys Chem Lett. 2024 Jul 11;15(27):6935-6942. doi: 10.1021/acs.jpclett.4c00164. Epub 2024 Jun 27.
4
CD1 and iNKT cells mediate immune responses against the GBS hemolytic lipid toxin induced by a non-toxic analog.
PLoS Pathog. 2023 Jun 29;19(6):e1011490. doi: 10.1371/journal.ppat.1011490. eCollection 2023 Jun.
7
Group B Streptococcal Hemolytic Pigment Impairs Platelet Function in a Two-Step Process.
Cells. 2022 May 13;11(10):1637. doi: 10.3390/cells11101637.
8
Disseminated intravascular coagulation as a complication after transvenous lead extraction for defibrillator-associated endocarditis: A case report.
HeartRhythm Case Rep. 2022 Feb 10;8(5):330-334. doi: 10.1016/j.hrcr.2022.02.001. eCollection 2022 May.
9
Some Like It Hot.
J Innate Immun. 2021;13(6):321-322. doi: 10.1159/000520270. Epub 2021 Oct 26.
10
The Road Not Taken: Commensal or Virulent Pathogen.
J Innate Immun. 2020;12(4):275-276. doi: 10.1159/000509601. Epub 2020 Jun 25.

本文引用的文献

1
Interaction of the Human Contact System with Pathogens-An Update.
Front Immunol. 2018 Feb 26;9:312. doi: 10.3389/fimmu.2018.00312. eCollection 2018.
2
How I treat disseminated intravascular coagulation.
Blood. 2018 Feb 22;131(8):845-854. doi: 10.1182/blood-2017-10-804096. Epub 2017 Dec 18.
3
Streptococcus gallolyticus subsp. gallolyticus endocarditis isolate interferes with coagulation and activates the contact system.
Virulence. 2018 Jan 1;9(1):248-261. doi: 10.1080/21505594.2017.1393600. Epub 2017 Dec 26.
4
Pathogenesis of meningococcal purpura fulminans.
Pathog Dis. 2017 Apr 1;75(3). doi: 10.1093/femspd/ftx027.
5
Group B Streptococcal Toxic Shock Syndrome and covR/S Mutations Revisited.
Emerg Infect Dis. 2017 Jan;23(1):150-152. doi: 10.3201/eid2301.161063.
7
Coagulation factor XII induces pro-inflammatory cytokine responses in macrophages and promotes atherosclerosis in mice.
Thromb Haemost. 2017 Jan 5;117(1):176-187. doi: 10.1160/TH16-06-0466. Epub 2016 Oct 27.
8
Biofilm in group A streptococcal necrotizing soft tissue infections.
JCI Insight. 2016 Jul 7;1(10):e87882. doi: 10.1172/jci.insight.87882.
9
Phosphoglycerate Kinase-A Novel Streptococcal Factor Involved in Neutrophil Activation and Degranulation.
J Infect Dis. 2016 Dec 15;214(12):1876-1883. doi: 10.1093/infdis/jiw450. Epub 2016 Sep 28.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验