Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflammatory activity and innate immune evasion.
Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflammatory activity and innate immune evasion.
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DOI：
10.1186/s12866-015-0569-3
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发表时间：
2015-10-23
期刊：
影响因子：
4.2
通讯作者：
Ingalls RR
中科院分区：
文献类型：
--
作者：
He X;Liang Y;LaValley MP;Lai J;Ingalls RR
肺炎衣原体是一种常见的人类病原体，与上呼吸道和下呼吸道感染有关。也有人认为，肺炎梭菌感染可引发或促进多种慢性炎症，包括哮喘和动脉粥样硬化。已经从人类和动物中分离出了几株肺炎球菌，序列数据显示出明显的遗传保守性，这就没有回答为什么在一些呼吸道获得性感染后可能发生慢性炎症的问题。采用AR39和AO3在体外感染小鼠骨髓源性巨噬细胞和L929成纤维细胞，在体内经鼻内感染C57BL/6小鼠。我们对呼吸道分离物AR39和动脉粥样硬化分离物AO3进行了比较研究，以确定这两种菌株之间的细菌生长和宿主对感染的反应是否不同。我们观察到不同寄主细胞类型和生长温度的生长差异；然而，这两种菌株都能在体外形成斑块。宿主对呼吸道分离物的反应在体外（就炎症细胞因子诱导而言）和体内（通过使用呼吸道感染小鼠模型的临床反应和肺部炎症标志物来测量）都被发现更具炎症性。我们的数据表明，在急性呼吸道感染期间，肺炎球菌菌株的一个亚群能够逃避宿主的先天免疫防御。进一步研究宿主和病原体方面这些差异的遗传基础，可以增强我们对肺炎梭菌如何促进局部和远处慢性炎症发展的理解。
Chlamydia pneumoniae is a common human pathogen that is associated with upper and lower respiratory tract infections. It has also been suggested that C. pneumoniae infection can trigger or promote a number of chronic inflammatory conditions, including asthma and atherosclerosis. Several strains of C. pneumoniae have been isolated from humans and animals, and sequence data demonstrates marked genetic conservation, leaving unanswered the question as to why chronic inflammatory conditions may occur following some respiratory-acquired infections. C. pneumoniae strains AR39 and AO3 were used in vitro to infect murine bone marrow derived macrophages and L929 fibroblasts, or in vivo to infect C57BL/6 mice via the intranasal route. We undertook a comparative study of a respiratory isolate, AR39, and an atheroma isolate, AO3, to determine if bacterial growth and host responses to infection varied between these two strains. We observed differential growth depending on the host cell type and the growth temperature; however both strains were capable of forming plaques in vitro. The host response to the respiratory isolate was found to be more inflammatory both in vitro, in terms of inflammatory cytokine induction, and in vivo, as measured by clinical response and lung inflammatory markers using a mouse model of respiratory infection. Our data demonstrates that a subset of C. pneumoniae strains is capable of evading host innate immune defenses during the acute respiratory infection. Further studies on the genetic basis for these differences on both the host and pathogen side could enhance our understanding how C. pneumoniae contributes to the development chronic inflammation at local and distant sites.