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.2016 Sep 6;23(9):757-66.
doi: 10.1128/CVI.00071-16. Print 2016 Sep.

CCL19 as a Chemokine Risk Factor for Posttreatment Lyme Disease Syndrome: a Prospective Clinical Cohort Study

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CCL19 as a Chemokine Risk Factor for Posttreatment Lyme Disease Syndrome: a Prospective Clinical Cohort Study

John N Aucott et al. Clin Vaccine Immunol..

Abstract

Approximately 10% to 20% of patients optimally treated for early Lyme disease develop persistent symptoms of unknown pathophysiology termed posttreatment Lyme disease syndrome (PTLDS). The objective of this study was to investigate associations between PTLDS and immune mediator levels during acute illness and at several time points following treatment. Seventy-six participants with physician-documented erythema migrans and 26 healthy controls with no history of Lyme disease were enrolled. Sixty-four cytokines, chemokines, and inflammatory markers were measured at each visit for a total of 6 visits over 1 year. An operationalized definition of PTLDS incorporating symptoms and functional impact was applied at 6 months and 1 year following treatment completion, and clinical outcome groups were defined as the return-to-health, symptoms-only, and PTLDS groups. Significance analysis of microarrays identified 7 of the 64 immune mediators to be differentially regulated by group. Generalized logit regressions controlling for potential confounders identified posttreatment levels of the T-cell chemokine CCL19 to be independently associated with clinical outcome group. Receiver operating characteristic analysis identified a CCL19 cutoff of >111.67 pg/ml at 1 month following treatment completion to be 82% sensitive and 83% specific for later PTLDS. We speculate that persistently elevated CCL19 levels among participants with PTLDS may reflect ongoing, immune-driven reactions at sites distal to secondary lymphoid tissue. Our findings suggest the relevance of CCL19 both during acute infection and as an immunologic risk factor for PTLDS during the posttreatment phase. Identification of a potential biomarker predictor for PTLDS provides the opportunity to better understand its pathophysiology and to develop early interventions in the context of appropriate and specific clinical information.

Copyright © 2016, American Society for Microbiology. All Rights Reserved.

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Figures

FIG 1
FIG 1
Immune marker analysis of early Lyme disease cases and controls over time. Three clinical outcome groups were defined using a previously published definition of PTLDS incorporating both persistent symptoms and functional impact (25).
FIG 2
FIG 2
Identification of relevant immune mediators. Serum samples from participants with early Lyme disease and healthy controls were assayed for the presence of soluble mediators using an optimized multiplex-based assay system. Mediators with significant changes (q < 0.1%) are displayed as heat maps to visualize differences. All study time points are represented in panels A to F for healthy controls, those that returned to health, those that reported symptoms without functional impact, and those that met the criteria for PTLDS (25). (A) Mediators with significant changes (q < 0.1%) at the acute-phase, pretreatment visit; (B) mediators with significant changes (q < 0.1%) at the posttreatment follow-up visit 3 weeks later; (C) mediators with significant changes (q < 0.1%) at 1 month following treatment completion; (D) mediators with significant changes (q < 0.1%) at 3 months following treatment completion; (E) mediators with significant changes (q < 0.1%) at 6 months following treatment completion; (F) mediators with significant changes (q < 0.1%) at 1 year following treatment completion. CRP, C-reactive protein.
FIG 3
FIG 3
CCL19 levels are elevated in Lyme disease cases with PTLDS. Displayed are the median and interquartile range serum levels of CCL19 among 76 Lyme disease patients over time. Lyme disease-exposed participants are divided into the PTLDS, symptoms-only, and return-to-health clinical outcome groups on the basis of self-reported symptoms and survey measurements at 6 months and 1 year posttreatment (25). The median control value (79.28 pg/ml; interquartile range, 62.60 to 114.85 pg/ml) is represented by a triangle in the graph. *,P ≤ 0.05 for comparison of each group to the controls; **,P ≤ 0.01 for comparison of each group to the controls.
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