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Infection and Immunity, April 2006, p. 2154-2160, Vol. 74, No. 4
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.4.2154-2160.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

MyD88 Deficiency Enhances Acquisition and Transmission of Borrelia burgdorferi by Ixodes scapularis Ticks

Linda K. Bockenstedt,1* Nengyin Liu,1 Ira Schwartz,2 and Durland Fish3

Department of Internal Medicine,1 Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520,3 Department of Microbiology and Immunology, New York Medical College, Valhalla, New York 105952

Received 1 December 2005/ Returned for modification 2 January 2006/ Accepted 18 January 2006

Borrelia burgdorferi strains exhibit various degrees of infectivity and pathogenicity in mammals, which may be due to their relative ability to evade initial host immunity. Innate immune cells recognize B. burgdorferi by Toll-like receptors (TLRs) that use the intracellular molecule MyD88 to mediate effector functions. To determine whether impaired TLR signaling enhances Ixodes scapularis acquisition of B. burgdorferi, we fed nymphs on wild-type (WT) and MyD88–/– mice previously infected with two clinical isolates of B. burgdorferi, BL206, a high-virulence strain, and B348, an attenuated strain. Seventy-three percent of the nymphs that fed on BL206-infected WT mice and 40% of the nymphs that fed on B348-infected WT mice acquired B. burgdorferi, whereas 100% of the nymphs that fed on MyD88–/– mice became infected, irrespective of B. burgdorferi strain. Ticks that acquired infection after feeding on MyD88–/– mice harbored more spirochetes than those that fed on WT mice, as assessed by quantitative PCR for B. burgdorferi DNA. Vector transmission of BL206 and B348 was also enhanced when MyD88–/– mice were the blood meal hosts, with the mean pathogen burden at the skin inoculation site significantly higher than levels in WT mice. These results show that the absence of MyD88 facilitates passage of both low- and high-infectivity B. burgdorferi strains between the tick vector and the mammal and enhances the infectivity of a low-infectivity B. burgdorferi strain.

* Corresponding author. Mailing address: S-525C TAC, Section of Rheumatology, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520-8031. Phone: (203) 785-2454. Fax: (203) 785-7053. E-mail: linda.bockenstedt{at}yale.edu.

Editor: D. L. Burns

Infection and Immunity, April 2006, p. 2154-2160, Vol. 74, No. 4
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.4.2154-2160.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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