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2型血清型生物膜抑制中性粒细胞胞外陷阱的形成。

Serotype 2 Biofilms Inhibit the Formation of Neutrophil Extracellular Traps.

作者信息

Ma Fang, Yi Li, Yu Ningwei, Wang Guangyu, Ma Zhe, Lin Huixing, Fan Hongjie

机构信息

College of Veterinary Medicine, Nanjing Agricultural University Nanjing, China.

College of Veterinary Medicine, Nanjing Agricultural UniversityNanjing, China; College of Life Science, Luoyang Normal UniversityLuoyang, China.

出版信息

Front Cell Infect Microbiol. 2017 Mar 20;7:86. doi: 10.3389/fcimb.2017.00086. eCollection 2017.

Abstract

Invasive infections caused by serotype 2 (SS2) has emerged as a clinical problem in recent years. Neutrophil extracellular traps (NETs) are an important mechanism for the trapping and killing of pathogens that are resistant to phagocytosis. Biofilm formation can protect bacteria from being killed by phagocytes. Until now, there have only been a few studies that focused on the interactions between bacterial biofilms and NETs. SS2 in both a biofilm state and a planktonic cell state were incubated with phagocytes and NETs, and bacterial survival was assessed. DNase I and cytochalasin B were used to degrade NET DNA or suppress phagocytosis, respectively. Extracellular DNA was stained with impermeable fluorescent dye to quantify NET formation. Biofilm formation increased up to 6-fold in the presence of neutrophils, and biofilms were identified in murine tissue. Both planktonic and biofilm cells induced neutrophils chemotaxis to the infection site, with neutrophils increasing by 85.1 and 73.8%, respectively. The bacteria in biofilms were not phagocytized. The bactericidal efficacy of NETs on the biofilms and planktonic cells were equal; however, the biofilm extracellular matrix can inhibit NET release. Although biofilms inhibit NETs release, NETs appear to be an important mechanism to eliminate SS2 biofilms. This knowledge advances the understanding of biofilms and may aid in the development of treatments for persistent infections with a biofilm component.

摘要

近年来,2型猪链球菌(SS2)引起的侵袭性感染已成为一个临床问题。中性粒细胞胞外陷阱(NETs)是捕获和杀死抗吞噬病原体的重要机制。生物膜形成可保护细菌不被吞噬细胞杀死。到目前为止,仅有少数研究关注细菌生物膜与NETs之间的相互作用。将处于生物膜状态和浮游细胞状态的SS2与吞噬细胞和NETs一起孵育,并评估细菌存活情况。分别使用脱氧核糖核酸酶I和细胞松弛素B降解NET DNA或抑制吞噬作用。用不透性荧光染料对细胞外DNA进行染色以定量NET形成。在中性粒细胞存在的情况下,生物膜形成增加至6倍,并且在小鼠组织中鉴定出生物膜。浮游细胞和生物膜细胞均诱导中性粒细胞向感染部位趋化,中性粒细胞分别增加85.1%和73.8%。生物膜中的细菌未被吞噬。NETs对生物膜和浮游细胞的杀菌效力相同;然而,生物膜细胞外基质可抑制NET释放。尽管生物膜抑制NETs释放,但NETs似乎是消除SS2生物膜的重要机制。这一认识增进了对生物膜的理解,并可能有助于开发针对具有生物膜成分的持续性感染的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af4f/5357632/584b6de49b2b/fcimb-07-00086-g0001.jpg

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