Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Upcoming)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Antiphospholipid autoantibodies in Lyme disease arise after scavenging of host phospholipids by Borrelia burgdorferi
Peter J. Gwynne, … , Adriana R. Marques, Linden T. Hu
Peter J. Gwynne, … , Adriana R. Marques, Linden T. Hu
Published March 15, 2022
Citation Information: J Clin Invest. 2022;132(6):e152506. https://doi.org/10.1172/JCI152506.
View: Text | PDF
Research Article Infectious disease Microbiology

Antiphospholipid autoantibodies in Lyme disease arise after scavenging of host phospholipids by Borrelia burgdorferi

  • Text
  • PDF
Abstract

A close association with its vertebrate and tick hosts allows Borrelia burgdorferi, the bacterium responsible for Lyme disease, to eliminate many metabolic pathways and instead scavenge key nutrients from the host. A lipid-defined culture medium was developed to demonstrate that exogenous lipids are an essential nutrient of B. burgdorferi, which can accumulate intact phospholipids from its environment to support growth. Antibody responses to host phospholipids were studied in mice and humans using an antiphospholipid ELISA. Several of these environmentally acquired phospholipids including phosphatidylserine and phosphatidic acid, as well as borrelial phosphatidylcholine, are the targets of antibodies that arose early in infection in the mouse model. Patients with acute infections demonstrated antibody responses to the same lipids. The elevation of antiphospholipid antibodies predicted early infection with better sensitivity than did the standardized 2-tier tests currently used in diagnosis. Sera obtained from patients with Lyme disease before and after antibiotic therapy showed declining antiphospholipid titers after treatment. Further study will be required to determine whether these antibodies have utility in early diagnosis of Lyme disease, tracking of the response to therapy, and diagnosis of reinfection, areas in which current standardized tests are inadequate.

Authors

Peter J. Gwynne, Luke H. Clendenen, Siu-Ping Turk, Adriana R. Marques, Linden T. Hu

×

Figure 1

Growth of B. burgdorferi is dependent upon exogenous lipids.

Options: View larger image (or click on image) Download as PowerPoint
Growth of B. burgdorferi is dependent upon exogenous lipids.
(A) Growth ...
(A) Growth of B. burgdorferi in lipid-free medium supplemented with fatty acids and cholesterol (2:2:1 palmitic acid/oleic acid/cholesterol) to a final concentration of 5–500 μM. At 500 μM, cell density equivalent to that of the unmodified BSK medium was reached. No growth was observed in the absence of lipid (dBSK only). (B) Equivalent growth over 10 days of B. burgdorferi in medium supplemented with fatty acids (FA) (200 μM each of palmitic and oleic acids) and phospholipids (PL) (100 μM each of PG and PC). Cholesterol (Ch) was present at 100 μM in all media. Data plotted in A and B show the mean of 3 biological replicates, with error bars indicating the SD.

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts