Metabolomics

, 12:74

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

Authors

  • Shradha Wali
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
  • Rishein Gupta
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
  • Jieh-Juen Yu
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
  • Adelphe Mfuh
    • Department of ChemistryUniversity of Texas at San Antonio
  • Xiaoli Gao
    • Department of BiochemistryUniversity of Texas Health Science Center at San Antonio
  • M. Neal Guentzel
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
  • James P. Chambers
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
  • Sazaly Abu Bakar
    • Department of Medical Microbiology, Faculty of MedicineUniversity of Malaya
  • Guangming Zhong
    • Department of Microbiology and ImmunologyUniversity of Texas Health Science Center at San Antonio
    • South Texas Center for Emerging Infectious Diseases and Center for Excellence in Infection GenomicsUniversity of Texas at San Antonio
Original Article

DOI: 10.1007/s11306-016-0998-5

Cite this article as:
Wali, S., Gupta, R., Yu, J. et al. Metabolomics (2016) 12: 74. doi:10.1007/s11306-016-0998-5

Abstract

Introduction

Chlamydia 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.

Objectives

The objective of this study was to determine the contribution of host metabolites in genital Ct infection.

Methods

We 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.

Results

Across 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.

Conclusion

This study demonstrates a role for host metabolite, PC 16:0/18:1 in regulating genital Ct infection in vivo and in vitro.

Keywords

Guinea pigChlamydia trachomatis serovar DIntravaginal infectionLipidsPhosphatidylcholine

Supplementary material

11306_2016_998_MOESM1_ESM.tif (634 kb)
Fig. S1PCA of Chlamydia trachomatis infected guinea pigs. Clusters obtained by principal component analysis (PCA) of log-scaled polar metabolite data of genital swabs obtained from Ct D and mock infected guinea pigs at days (a) 3, (b) 9 and (c) 15 post challenge. Supplementary material 1 (TIFF 634 kb)
11306_2016_998_MOESM2_ESM.docx (29 kb)
Table S1Fold changes in representative species detected in various metabolite families following Chlamydia trachomatis D infection In vivo (swabs obtained from guinea pigs). Supplementary material 2 (DOCX 28 kb)

Copyright information

© Springer Science+Business Media New York 2016