CCL17 influences Borrelia burgdorferi infection in the heart

Xiaotian Tang; Qian Yu; Yingjun Cui; Thomas M Hart; Freddie Rivas-Giorgi; Keith Calloway; Amrita Ray Mohapatra; Erol Fikrig

doi:10.1093/infdis/jiaf011

CCL17 influences Borrelia burgdorferi infection in the heart

J Infect Dis. 2025 Jan 8:jiaf011. doi: 10.1093/infdis/jiaf011. Online ahead of print.

Authors

Xiaotian Tang^{1

2}, Qian Yu², Yingjun Cui², Thomas M Hart², Freddie Rivas-Giorgi³, Keith Calloway², Amrita Ray Mohapatra², Erol Fikrig²

Affiliations

¹ Zhejiang Key Laboratory of Biology and Ecological Regulation of Crop Pathogens and Insects, Ministry of Agriculture Key Lab of Molecular Biology of Crop Pathogens and Insect Pests, Institute of Insect Sciences, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310030, China.
² Section of Infectious Diseases, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT 06510, USA.
³ Molecular Biochemistry & Biophysics Program, Yale College, New Haven, CT 06510, USA.

PMID: 39777514
DOI: 10.1093/infdis/jiaf011

Abstract

Lyme disease, caused by Borrelia burgdorferi, is transmitted to humans by Ixodes ticks. CCL17 is a potent chemokine that plays important roles in diverse illnesses, including autoimmune and infectious diseases. CCL17 knockout (KO) mice, infected with B. burgdorferi, had a reduced pathogen load in the heart, compared to control animals. Mice lacking CCL17 also showed signs of immune alteration upon B. burgdorferi infection, including diverse serum levels of proinflammatory cytokines and fewer monocytes and macrophages infiltration. CCL17 also interacts directly with B. burgdorferi, the first demonstration that this chemokine has an affinity for a vector-borne pathogen.

Keywords: Borrelia burgdorferi; CCL17; Heart; Infection; Lyme disease.

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