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. 2018 Feb 23;13(2):e0193424.
doi: 10.1371/journal.pone.0193424. eCollection 2018.

Lipidomic analysis of immune activation in equine leptospirosis and Leptospira-vaccinated horses

Paul L Wood  1 , Margaret Steinman  2 , Erdal Erol  2 , Craig Carter  2 , Undine Christmann  3 , Ashutosh Verma  3
Affiliations

Lipidomic analysis of immune activation in equine leptospirosis and Leptospira-vaccinated horses

Paul L Wood et al. PLoS One. .

Abstract

Currently available diagnostic assays for leptospirosis cannot differentiate vaccine from infection serum antibody. Several leptospiral proteins that are upregulated during infection have been described, but their utility as a diagnostic marker is still unclear. In this study, we undertook a lipidomics approach to determine if there are any differences in the serum lipid profiles of horses naturally infected with pathogenic Leptospira spp. and horses vaccinated against a commercially available bacterin. Utilizing a high-resolution mass spectrometry serum lipidomics analytical platform, we demonstrate that cyclic phosphatidic acids, diacylglycerols, and hydroperoxide oxidation products of choline plasmalogens are elevated in the serum of naturally infected as well as vaccinated horses. Other lipids of interest were triacylglycerols that were only elevated in the serum of infected horses and sphingomyelins that were increased only in the serum of vaccinated horses. This is the first report looking at the equine serum lipidome during leptospiral infection and vaccination.

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Conflict of interest statement

Competing Interests: All authors have no competing interests.

Figures

Fig 1
Fig 1. Equine serum levels of cyclic phosphatidic acid 16:0 (cPA) in a pilot study (N = 6 per group) and a validation study (N = 15 per group).
Con: controls; Vacc: vaccinated; Infect: infected. *, p < 0.01. R = ratio of the ion intensity for the endogenous cPA to the ion intensity of the stable isotope internal standard.
Fig 2
Fig 2. Equine serum levels of cyclic phosphatidic acids (cPA 16:0, cPA 18:0, cPA 18:1, and cPA 18:2) and lysophosphatidylcholines (LPC16:0, LPC 18:0, LPC 18:1, and LPC 18:2) in the validation study (N = 15 per group).
Con: controls; Vacc: vaccinated; Infect: infected. *, p < 0.01 vs. controls; #, p < 0.01 vs. the vaccinated cohort. R = ratio of the ion intensity for the endogenous cPA or LPC to the ion intensity of the stable isotope internal standard.
Fig 3
Fig 3. Biosynthetic pathway for cyclic phosphatidic acids (cPA).
LPC: lysophosphatidyl-choline; PLA2: phospholipase A2; PLD: phospholipase D; PtdC: phosphatidylcholine. ppm, parts per million mass error.
Fig 4
Fig 4. Equine serum levels of diacylglycerol 36:2 (DAG 36:2) and triacylglycerol 50:4 (TAG 50:4) in a pilot study (N = 6 per group) and a validation study (N = 15 per group).
Con: controls; Vacc: vaccinated; Infect: infected. *, p < 0.01. R = ratio of the ion intensity for the endogenous TAG to the ion intensity of the stable isotope internal standard.
Fig 5
Fig 5. Equine serum levels of sphingomyelins (SM), SM d18:1/24:0 and SM d18:1:24:2 in a pilot study (N = 6 per group) and a validation study (N = 15 per group).
Con: controls; Vacc: vaccinated; Infect: infected. *, p < 0.01. R = ratio of the ion intensity for the endogenous SM to the ion intensity of the stable isotope internal standard.
Fig 6
Fig 6. Equine serum levels of choline plasmalogen (PlsC) hydroperoxides (N = 15 per group).
Con: controls; Vacc: vaccinated; Infect: infected. *, p < 0.01; **, p < 0.05. R = ratio of the ion intensity for the endogenous hydroperoxide to the ion intensity of the stable isotope internal standard.
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