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【bio-news】血小板在败血症中促进中性粒细胞形成
Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood.Clark SR, Ma AC, Tavener SA, McDonald B, Goodarzi Z, Kelly MM, Patel KD, Chakrabarti S, McAvoy E, Sinclair GD, Keys EM, Allen-Vercoe E, Devinney R, Doig CJ, Green FH, Kubes P.
[1] Department of Physiology and Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada. [2] These authors contributed equally to this work.
It has been known for many years that neutrophils and platelets participate in the pathogenesis of severe sepsis, but the inter-relationship between these players is completely unknown. We report several cellular events that led to enhanced trapping of bacteria in blood vessels: platelet TLR4 detected TLR4 ligands in blood and induced platelet binding to adherent neutrophils. This led to robust neutrophil activation and formation of neutrophil extracellular traps (NETs). Plasma from severely septic humans also induced TLR4-dependent platelet-neutrophil interactions, leading to the production of NETs. The NETs retained their integrity under flow conditions and ensnared bacteria within the vasculature. The entire event occurred primarily in the liver sinusoids and pulmonary capillaries, where NETs have the greatest capacity for bacterial trapping. We propose that platelet TLR4 is a threshold switch for this new bacterial trapping mechanism in severe sepsis.
PMID: 17384648 [PubMed - in process] 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 Nat Med. 2007 Apr;13(4):463-9. Epub 2007 Mar 25. Links
自然医学 2007年 4月 第13卷第4期：463-469页，电子出版于2007年3月25日 说明：编译含有部分背景资料！
背景资料：
第一个背景资料英文及中文。
http://www.medicalnewstoday.com/medicalnews.php?newsid=60571
A Beneficial Suicide
Main Category: Blood / Hematology News
Article Date: 15 Jan 2007 - 11:00 PDT
They are the largest group of white blood cells: neutrophil granulocytes kill microorganisms. Neutrophils catch microbes with extracellular structures nicknamed Neutrophil Extracellular Traps (NETs) that are composed of nucleic acid and aggressive enzymes. A group of scientists lead by Arturo Zychlinsky at the Max-Planck-Institute for Infectious Biology in Berlin, Germany discovered, how the neutrophils form this snaring network (Journal of Cell Biology, online, January 8, 2007 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed 下文 ). Once triggered, the cells undergo a novel program leading to their death. While they perish, the cells release the content of their nuclei. The nucleic acid, mingled with bactericidal enzymes, forms a lethal network outside the cell. Invading bacteria and pathogenic fungi get caught and killed in the NETs.
Every minute, several million neutrophils leave the bone marrow and are ready to defend the body of invading germs. They are the immune system's first line of defence against harmful bacteria and migrate into the tissue at the site of infection to combat pathogens. For more than hundred years it was known that neutrophil granulocytes kill bacteria very efficiently by devouring them. After eating the germs neutrophils kill tehm with antimicrobial proteins.
The group of scientists lead by Arturo Zychlinsky at the Max-Planck-Institute for Infectious Biology discovered a second killing mechanism: neutrophil granulocytes can form web-like structures outside the cells composed of nucleic acid and enzymes which catch bacteria and kill them. The scientists were able to generate impressive micrographs of these nets. But it remained a mystery how the granulocytes could mobilise the contents of their nuclei and catapult it out of the cells.
Only after lengthy live cell imaging and biochemical studies it became clear how neutrophils make NETs. The cells get activated by bacteria and modify the structure of their nuclei and granules, small enzyme deposits in the cytoplasm. "The nuclear membrane disintegrates, the granules dissolve, and thus the NET components can mingle inside the cells", explains Volker Brinkmann, head of the microscopy group. At the end of this process, the cell contracts until the cell membrane bursts open and quickly releases the highly active melange. Once outside the cell, it unfolds and forms the NETs which then can trap bacteria.
Surprisingly, this process is as effective as devouring bacteria: "NETs formed by dying granulocytes kill as many bacteria as are eaten up by living blood cells", says Arturo Zychlinsky. Thus, neutrophils fulfil their role in the defence battle even after their deaths.
它们是数量最多的白细胞种类：能够杀死微生物的中性粒细胞。绰号Neutrophil Extracellular Traps (NETs)的结构是中性粒细胞的细胞外结构，由核苷酸和侵袭性酶组成，具有捕获微生物的作用。来自德国柏林马克斯普朗克传染生物学研究所的Arturo Zychlinsky带领一组研究团队，揭示了中性粒细胞形成这种捕捉结构的机制(《细胞生物学杂志》，网络版，2007年1月8日)。中性粒细胞一经触发就会产生自杀行为，并在死亡时释放其原子核内容物（核苷酸）。核苷酸与杀菌酶混合在一起，从而在中性粒细胞外形成了一个致命结构，捕获并杀死入侵的细菌和致病性真菌。
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作者:admin@医学,生命科学 2010-10-23 05:11
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