Guinea pig genital tract lipidome reveals in vivo and in vitro regulation of phosphatidylcholine 16:0/18:1 and contribution to Chlamydia trachomatis serovar D infectivity.
Guinea pig genital tract lipidome reveals in vivo and in vitro regulation of phosphatidylcholine 16:0/18:1 and contribution to Chlamydia trachomatis serovar D infectivity.
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豚鼠生殖道脂质组揭示了磷脂酰胆碱 16:0/18:1 的体内和体外调节以及对沙眼衣原体 D 血清型感染性的贡献。
DOI：
10.1007/s11306-016-0998-5
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发表时间：
2016
期刊：
影响因子：
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通讯作者：
Arulanandam,BernardP
中科院分区：
文献类型：
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作者：
Wali,Shradha;Gupta,Rishein;Yu,Jieh-Juen;Mfuh,Adelphe;Gao,Xiaoli;Guentzel,MNeal;Chambers,JamesP;AbuBakar,Sazaly;Zhong,Guangming;Arulanandam,BernardP
沙眼衣原体（Chlamydia trachomatis，Ct）是导致全球性传播疾病的主要病原体。宿主转录组学或蛋白质组学分析研究已经确定了参与建立Ct感染或产生抗Ct免疫的关键分子。然而，宿主代谢物组的贡献是未知的。ObjectivesThe的目的，这项研究的目的是要确定的贡献，在生殖器Ct infection.MethodsWe使用高效液相色谱-质谱，并映射脂质配置文件在生殖器拭子从雌性豚鼠在第3天，第9天，第15天，第30天和第65天后Ct血清型D阴道内infection.ResultsAcross所有时间点评估，检测到13种不同的脂质物质，包括胆碱、乙醇胺和甘油。在这些代谢物中，磷脂酰胆碱（PC）是从主动脱落细菌的动物中检测到的主要磷脂，即，在感染后3、9和15天。然而，在第30天和第65天，当动物清除感染时，观察到PC与先前时间点相比降低。豚鼠（体内）和104 C1豚鼠细胞系（体外）中产生的PC的质谱分析揭示了Ct D感染后不同的PC种类。其中，在本报告中研究的体内和体外感染模型中，PC 16：0/18：1在Ct D感染后显著上调（p< 0.05，>两倍变化）。外源性PC 16：0/18：1的加入导致Hela 229 cells.ConclusionThis study demonstrates a role for host metabolism，PC 16：0/18：1 in regulating genital Ct infection in vivo and in vitro.
IntroductionChlamydia trachomatis(Ct), is the leading cause of sexually transmitted infections worldwide. Host transcriptomic- or proteomic profiling studies have identified key molecules involved in establishment of Ct infection or the generation of anti Ct-immunity. However, the contribution of the host metabolome is not known.ObjectivesThe objective of this study was to determine the contribution of host metabolites in genital Ct infection.MethodsWe used high-performance liquid chromatography-mass spectrometry, and mapped lipid profiles in genital swabs obtained from female guinea pigs at days 3, 9, 15, 30 and 65 post Ct serovar D intravaginal infection.ResultsAcross all time points assessed, 13 distinct lipid species including choline, ethanolamine and glycerol were detected. Amongst these metabolites, phosphatidylcholine (PC) was the predominant phospholipid detected from animals actively shedding bacteria i.e., at 3, 9, and 15 days post infection. However, at days 30 and 65 when the animals had cleared the infection, PC was observed to be decreased compared to previous time points. Mass spectrometry analyses of PC produced in guinea pigs (in vivo) and 104C1 guinea pig cell line (in vitro) revealed distinct PC species following Ct D infection. Amongst these, PC 16:0/18:1 was significantly upregulated following Ct D infection (p< 0.05, >twofold change) in vivo and in vitro infection models investigated in this report. Exogenous addition of PC 16:0/18:1 resulted in significant increase in Ct D in Hela 229 cells.ConclusionThis study demonstrates a role for host metabolite, PC 16:0/18:1 in regulating genital Ct infection in vivo and in vitro.