CCL17 chemokine plays a significant role in modulating Borrelia burgdorferi infection in cardiac tissue. CCL17 knockout mice exhibited reduced cardiac pathogen load and altered immune responses, including decreased monocyte and macrophage infiltration and changes in proinflammatory cytokine levels.
Background
Lyme disease, caused by the spirochete Borrelia burgdorferi and transmitted by Ixodes ticks, is the most common vector-borne infection in North America. While antibiotics effectively treat most cases, some patients develop persistent symptoms including carditis. Host factors such as cytokines and chemokines influence disease pathogenesis. CCL17, a chemokine involved in inflammatory and infectious diseases, has been implicated in cardiac conditions and infectious processes, prompting investigation into its role in Lyme carditis.
Data Highlights
Parameter
Wild-Type Mice
CCL17 Knockout Mice
Cardiac B. burgdorferi Load
Higher
Reduced
Monocyte and Macrophage Infiltration in Heart
Increased
Decreased
Serum Proinflammatory Cytokine Levels
Elevated
Altered (varied)
Key Findings
CCL17 knockout mice infected with B. burgdorferi showed significantly reduced pathogen burden in cardiac tissue compared to wild-type controls.
Loss of CCL17 resulted in decreased infiltration of monocytes and macrophages into the heart during infection.
Serum levels of proinflammatory cytokines were altered in CCL17-deficient mice, indicating immune modulation.
CCL17 directly interacts with B. burgdorferi, representing the first evidence of this chemokine binding a vector-borne pathogen.
CCL17 expression is induced by B. burgdorferi antigens and is associated with cardiac infection severity.
Clinical Implications
These findings suggest that CCL17 contributes to the pathogenesis of Lyme carditis by modulating immune cell recruitment and inflammatory responses in the heart. Targeting CCL17 may represent a novel therapeutic strategy to reduce cardiac complications in Lyme disease. Understanding CCL17’s interaction with B. burgdorferi could inform development of interventions to modulate host-pathogen interactions.
Conclusion
CCL17 plays a critical role in mediating cardiac infection and immune responses during Borrelia burgdorferi infection. Its direct interaction with the pathogen and influence on immune cell dynamics highlight CCL17 as a potential target for therapeutic intervention in Lyme carditis.
References
Feng et al 2024 -- The Role of CCL17 in Modulating Borrelia burgdorferi Infection in Cardiac Tissue
