The Vsa proteins modulate susceptibility of mycoplasma pulmonis to complement killing, hemadsorption, and adherence to polystyrene

The Vsa proteins modulate susceptibility of mycoplasma pulmonis to complement killing, hemadsorption, and adherence to polystyrene
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DOI:
10.1128/iai.71.10.5733-5738.2003
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发表时间:
2003-10-01
影响因子:
3.1
通讯作者:
Dybvig, K
Dybvig, K
中科院分区:
医学2区
文献类型:
--
作者:
Simmons, WL;Dybvig, K

文献摘要

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小鼠呼吸道病原体肺支原体的可变表面抗原(Vsa)与肺中微生物的毒力有关。在菌株UAB CT中,抗原由一个n端区域组成,该区域与串联重复序列组成的七个不同的c端可变区域之一结合。肺分枝杆菌产生的VsaA蛋白约有40个串联重复序列(1140),不粘附在红细胞或聚苯乙烯上。产生VsaH的菌株含有缺乏串联重复序列的短c端区域,并粘附在红细胞和塑料上。我们分离并分析了肺分枝杆菌菌株CT变体(CT182及其衍生物),这些变体仅产生三个串联重复序列(W)的VsaA蛋白。这些变异与产生vsah的菌株类似地粘附在塑料和红细胞上。产r3的CT182菌株和产vsah的菌株与正常豚鼠血清孵育后,均被有效杀灭。当血清被热灭活时,杀戮就被废除了。相比之下,产生VsaA R40的肺分枝杆菌菌株对补体杀伤具有高度抗性。在补体杀伤反应中存活下来的CT182R3变体都产生R40形式的VsaA,并且对补体杀伤具有抗性。VsaA R40是首个被证实与补体耐药性相关的支原体蛋白。由于vsaah和VsaA都可以介导对塑料的粘附、细胞粘附和对补体的易感性,我们提出Vsa通过非特异性相互作用调节这些表型。
The variable surface antigens (Vsa) of the murine respiratory pathogen Mycoplasma pulmonis are associated with the virulence of the microorganism in the lung. In strain UAB CT, the antigens consist of an N-terminal region that is combined with one of seven different C-terminal variable regions comprised of tandem repeats. M. pulmonis producing a VsaA protein with about 40 tandem repeats (1140) does not adhere to red blood cells or polystyrene. Strains that produce VsaH contain a short C-terminal region that lacks tandem repeats and adhere to red blood cells and plastic. We isolated and analyzed M. pulmonis strain CT variants (CT182 and derivatives) that produced a VsaA protein with only three tandem repeats (W). These variants adhered to plastic and red blood cells similarly to the VsaH-producing strain. When the R3-producing CT182 strain or the VsaH-producing strains were incubated with normal guinea pig serum, they were efficiently killed. Killing was abolished when the serum was heat inactivated. In contrast, the M. pulmonis strains that produced VsaA R40 were highly resistant to complement killing. CT182R3 variants that survived the complement killing reactions all produced the R40 form of VsaA and were resistant to complement killing. VsaA R40 is the first mycoplasmal protein shown to be associated with resistance to complement. As both VsaH and VsaA can mediate adherence to plastic, cytadherence, and susceptibility to complement, we propose that Vsa modulates these phenotypes by nonspecific interactions.