SCGB1D2 inhibits growth of Borrelia burgdorferi and affects susceptibility to Lyme disease

Satu Strausz, Erik Abner, Grace Blacker, Sarah Galloway, Paige Hansen, Qingying Feng, Brandon T. Lee, Samuel E. Jones, Hele Haapaniemi, Sten Raak, George Ronald Nahass, Erin Sanders, Pilleriin Soodla, Urmo Võsa, Tõnu Esko, Nasa Sinnott-Armstrong, Irving L. Weissman, Mark Daly, Tuomas Aivelo, Michal Caspi Tal () and Hanna M. Ollila ()
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Satu Strausz: Helsinki Institute of Life Science, University of Helsinki
Erik Abner: Institute of Genomics, University of Tartu
Grace Blacker: Stanford University School of Medicine
Sarah Galloway: Stanford University School of Medicine
Paige Hansen: Stanford University School of Medicine
Qingying Feng: Massachusetts Institute of Technology
Brandon T. Lee: Stanford University School of Medicine
Samuel E. Jones: Helsinki Institute of Life Science, University of Helsinki
Hele Haapaniemi: Helsinki Institute of Life Science, University of Helsinki
Sten Raak: Institute of Genomics, University of Tartu
George Ronald Nahass: Stanford University School of Medicine
Erin Sanders: Stanford University School of Medicine
Pilleriin Soodla: Internal Medicine Clinic, Tartu University Hospital
Urmo Võsa: Institute of Genomics, University of Tartu
Tõnu Esko: Institute of Genomics, University of Tartu
Nasa Sinnott-Armstrong: Helsinki Institute of Life Science, University of Helsinki
Irving L. Weissman: Stanford University School of Medicine
Mark Daly: Helsinki Institute of Life Science, University of Helsinki
Tuomas Aivelo: University of Helsinki
Michal Caspi Tal: Stanford University School of Medicine
Hanna M. Ollila: Helsinki Institute of Life Science, University of Helsinki

Nature Communications, 2024, vol. 15, issue 1, 1-11

Abstract: Abstract Lyme disease is a tick-borne disease caused by bacteria of the genus Borrelia. The host factors that modulate susceptibility for Lyme disease have remained mostly unknown. Using epidemiological and genetic data from FinnGen and Estonian Biobank, we identify two previously known variants and an unknown common missense variant at the gene encoding for Secretoglobin family 1D member 2 (SCGB1D2) protein that increases the susceptibility for Lyme disease. Using live Borrelia burgdorferi (Bb) we find that recombinant reference SCGB1D2 protein inhibits the growth of Bb in vitro more efficiently than the recombinant protein with SCGB1D2 P53L deleterious missense variant. Finally, using an in vivo murine infection model we show that recombinant SCGB1D2 prevents infection by Borrelia in vivo. Together, these data suggest that SCGB1D2 is a host defense factor present in the skin, sweat, and other secretions which protects against Bb infection and opens an exciting therapeutic avenue for Lyme disease.

Date: 2024
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DOI: 10.1038/s41467-024-45983-9

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