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本文引用的文献

1
Comparative genomic analyses of attenuated strains of Mycoplasma gallisepticum.鸡毒支原体减毒株的比较基因组分析。
Infect Immun. 2010 Apr;78(4):1760-71. doi: 10.1128/IAI.01172-09. Epub 2010 Feb 1.
2
Impact of genome reduction on bacterial metabolism and its regulation.基因组缩减对细菌代谢及其调控的影响。
Science. 2009 Nov 27;326(5957):1263-8. doi: 10.1126/science.1177263.
3
Characterization of a unique ADP-ribosyltransferase of Mycoplasma penetrans.穿透支原体独特的ADP核糖基转移酶的特性分析
Infect Immun. 2009 Oct;77(10):4362-70. doi: 10.1128/IAI.00044-09. Epub 2009 Aug 3.
4
Binding of IgA by Mycoplasma penetrans.穿透支原体与IgA的结合。
Curr Microbiol. 2009 Apr;58(4):360-5. doi: 10.1007/s00284-009-9359-1. Epub 2009 Feb 3.
5
Mycoplasma genitalium-encoded MG309 activates NF-kappaB via Toll-like receptors 2 and 6 to elicit proinflammatory cytokine secretion from human genital epithelial cells.生殖支原体编码的MG309通过Toll样受体2和6激活核因子κB,以引发人泌尿生殖上皮细胞分泌促炎细胞因子。
Infect Immun. 2009 Mar;77(3):1175-81. doi: 10.1128/IAI.00845-08. Epub 2008 Dec 22.
6
COBEpro: a novel system for predicting continuous B-cell epitopes.COBEpro:一种预测连续B细胞表位的新型系统。
Protein Eng Des Sel. 2009 Mar;22(3):113-20. doi: 10.1093/protein/gzn075. Epub 2008 Dec 10.
7
Mhp493 (P216) is a proteolytically processed, cilium and heparin binding protein of Mycoplasma hyopneumoniae.Mhp493(P216)是一种经蛋白水解处理的猪肺炎支原体纤毛和肝素结合蛋白。
Mol Microbiol. 2009 Feb;71(3):566-82. doi: 10.1111/j.1365-2958.2008.06546.x. Epub 2008 Dec 4.
8
Mutation of two Mycoplasma arthritidis surface lipoproteins with divergent functions in cytadherence.两种在细胞黏附中具有不同功能的关节炎支原体表面脂蛋白的突变。
Infect Immun. 2008 Dec;76(12):5768-76. doi: 10.1128/IAI.00160-08. Epub 2008 Sep 15.
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BMC Microbiol. 2008 Jul 23;8:124. doi: 10.1186/1471-2180-8-124.
10
A triacylated lipoprotein from Mycoplasma genitalium activates NF-kappaB through Toll-like receptor 1 (TLR1) and TLR2.来自生殖支原体的一种三酰化脂蛋白通过Toll样受体1(TLR1)和TLR2激活核因子κB。
Infect Immun. 2008 Aug;76(8):3672-8. doi: 10.1128/IAI.00257-08. Epub 2008 May 12.

鉴定脂蛋白 MslA 为鸡毒支原体的一种新型毒力因子。

Identification of lipoprotein MslA as a neoteric virulence factor of Mycoplasma gallisepticum.

机构信息

Center of Excellence for Vaccine Research, Department of Pathobiology and Veterinary Science, University of Connecticut, 61 N. Eagleville Rd., Storrs, CT 06269, USA.

出版信息

Infect Immun. 2010 Aug;78(8):3475-83. doi: 10.1128/IAI.00154-10. Epub 2010 Jun 1.

DOI:10.1128/IAI.00154-10
PMID:20515935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2916287/
Abstract

Many lipoproteins are expressed on the surfaces of mycoplasmas, and some have been implicated as playing roles in pathogenesis. Family 2 lipoproteins of Mycoplasma pneumoniae have a conserved "mycoplasma lipoprotein X" central domain and a "mycoplasma lipoprotein 10" C-terminal domain and are differentially expressed in response to environmental conditions. Homologues of family 2 lipoproteins are Mycoplasma specific and include the lipoprotein of Mycoplasma gallisepticum, encoded by the MGA0674 gene. Comparative transcriptomic analysis of the M. gallisepticum live attenuated vaccine strain F and the virulent strain R(low), reported in this study, indicated that MGA0674 is one of several differentially expressed genes. The MGA0674-encoded lipoprotein is a proteolytically processed, immunogenic, TX-114 detergent-phase protein which appears to have antigenic divergence between field strains R(low) and S6. We examined the virulence of an R(low) Delta MGA0674 mutant (P1H9) in vivo and observed reduced recovery and attenuated virulence in the tracheas of experimentally infected chickens. The virulence of two additional R(low) Delta MGA0674 mutants, 2162 and 2204, was assessed in a second in vivo virulence experiment. These mutants exhibited partial to complete attenuation in vivo, but recovery was observed more frequently. Since only Mycoplasma species harbor homologues of MGA0674, the gene product has been renamed "Mycoplasma-specific lipoprotein A" (MslA). Collectively, these data indicate that MslA is an immunogenic lipoprotein exhibiting reduced expression in an attenuated strain and plays a role in M. gallisepticum virulence.

摘要

许多脂蛋白在支原体表面表达,其中一些与发病机制有关。肺炎支原体家族 2 脂蛋白具有保守的“支原体脂蛋白 X”中心结构域和“支原体脂蛋白 10”C 末端结构域,并对环境条件表现出差异表达。家族 2 脂蛋白的同源物是支原体特异性的,包括禽支原体的脂蛋白,由 MGA0674 基因编码。本研究报道了对活减毒疫苗株 F 和毒力株 R(low)的比较转录组分析,表明 MGA0674 是几个差异表达基因之一。MGA0674 编码的脂蛋白是一种经蛋白水解处理的、免疫原性的 TX-114 去污剂相蛋白,似乎在现场菌株 R(low)和 S6 之间具有抗原分化。我们在体内研究了 R(low)Delta MGA0674 突变体(P1H9)的毒力,观察到在实验感染鸡的气管中恢复减少和毒力减弱。在第二个体内毒力实验中评估了另外两个 R(low)Delta MGA0674 突变体 2162 和 2204 的毒力。这些突变体在体内表现出部分至完全衰减,但恢复的情况更为频繁。由于只有支原体物种具有 MGA0674 的同源物,因此该基因产物已被重新命名为“支原体特异性脂蛋白 A”(MslA)。综上所述,这些数据表明 MslA 是一种免疫原性脂蛋白,在减毒菌株中表达减少,在禽支原体毒力中发挥作用。