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血小板活化因子受体缺陷型小鼠呼吸道中非分型流感嗜血杆菌的清除情况未发生改变。

Platelet-activating factor receptor-deficient mice show an unaltered clearance of nontypeable Haemophilus influenzae from their respiratory tract.

作者信息

Branger Judith, Wieland Catharina W, Florquin Sandrine, Maris Nico A, Pater Jennie M, Speelman Peter, Shimizu Takao, Ishii Satoshi, van der Poll Tom

机构信息

Department of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, The Netherlands.

出版信息

Shock. 2004 Dec;22(6):543-7. doi: 10.1097/01.shk.0000142818.91693.73.

DOI:10.1097/01.shk.0000142818.91693.73
PMID:15545826
Abstract

Platelet-activating factor (PAF), a glycerophospholipid with proinflammatory properties, exerts its biological effects by interacting with the PAF receptor (PAFR) expressed on many different cell types. The PAFR specifically binds phosphorylcholine, the biologically active component of PAF. However, phosphorylcholine is also a component of the cell wall of nontypeable Haemophilus influenzae (NTHi). In recently published in vitro experiments, the invasion of respiratory epithelial cells by NTHi was mediated by the PAFR. To determine the role of the PAFR in host defense against pneumonia induced by NTHi, PAFR-deficient (PAFR-/-) and normal wild-type mice were intranasally inoculated with NTHi. The absence of a functional PAFR was associated with a normal innate immune response as indicated by similar bacterial counts, myeloperoxidase activity, and inflammation within the pulmonary compartment of PAFR-/- and wild-type mice. These data indicate that the PAFR does not interfere with the clearance of NTHi from the respiratory tract.

摘要

血小板活化因子(PAF)是一种具有促炎特性的甘油磷脂,它通过与多种不同细胞类型上表达的PAF受体(PAFR)相互作用来发挥其生物学效应。PAFR特异性结合PAF的生物活性成分磷酰胆碱。然而,磷酰胆碱也是不可分型流感嗜血杆菌(NTHi)细胞壁的组成成分。在最近发表的体外实验中,NTHi对呼吸道上皮细胞的侵袭是由PAFR介导的。为了确定PAFR在宿主抵御NTHi诱导的肺炎中的作用,将PAF受体缺陷(PAFR-/-)小鼠和正常野生型小鼠经鼻接种NTHi。PAFR-/-小鼠和野生型小鼠肺内细菌计数、髓过氧化物酶活性及炎症反应相似,表明缺乏功能性PAFR与正常的固有免疫反应相关。这些数据表明,PAFR不会干扰呼吸道中NTHi的清除。

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Platelet-activating factor receptor-deficient mice show an unaltered clearance of nontypeable Haemophilus influenzae from their respiratory tract.血小板活化因子受体缺陷型小鼠呼吸道中非分型流感嗜血杆菌的清除情况未发生改变。
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引用本文的文献

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Molecules. 2018 Aug 8;23(8):1979. doi: 10.3390/molecules23081979.
2
Microbial modulation of host immunity with the small molecule phosphorylcholine.小分子磷酸胆碱对宿主免疫的微生物调节。
Infect Immun. 2013 Feb;81(2):392-401. doi: 10.1128/IAI.01168-12. Epub 2012 Dec 10.
3
Non-typeable Haemophilus influenzae invasion and persistence in the human respiratory tract.
无法分型流感嗜血杆菌在人体呼吸道中的入侵和持续存在。
Front Cell Infect Microbiol. 2011 Nov 18;1:1. doi: 10.3389/fcimb.2011.00001. eCollection 2011.
4
Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasion.A 群链球菌分泌的酯酶水解血小板激活因子,以阻止中性粒细胞的募集并促进先天免疫逃避。
PLoS Pathog. 2012;8(4):e1002624. doi: 10.1371/journal.ppat.1002624. Epub 2012 Apr 5.
5
Phosphorylcholine allows for evasion of bactericidal antibody by Haemophilus influenzae.磷酰胆碱使流感嗜血杆菌逃避杀菌抗体。
PLoS Pathog. 2012;8(3):e1002521. doi: 10.1371/journal.ppat.1002521. Epub 2012 Mar 1.
6
The platelet activating factor receptor is not required for exacerbation of bacterial pneumonia following influenza.流感后细菌性肺炎加重并不需要血小板活化因子受体。
Scand J Infect Dis. 2008;40(1):11-7. doi: 10.1080/00365540701477568. Epub 2007 Jun 21.
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Interleukin 18 participates in the early inflammatory response and bacterial clearance during pneumonia caused by nontypeable Haemophilus influenzae.白细胞介素18参与了由不可分型流感嗜血杆菌引起的肺炎期间的早期炎症反应和细菌清除过程。
Infect Immun. 2007 Oct;75(10):5068-72. doi: 10.1128/IAI.00287-07. Epub 2007 Jul 30.
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Inhalation of beta 2 agonists impairs the clearance of nontypable Haemophilus influenzae from the murine respiratory tract.吸入β2激动剂会损害无荚膜流感嗜血杆菌从鼠类呼吸道的清除。
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