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Infection and Immunity, September 2005, p. 5547-5553, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5547-5553.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi Organisms Lacking Plasmids 25 and 28-1 Are Internalized by Human Blood Phagocytes at a Rate Identical to That of the Wild-Type Strain

Samiya Al-Robaiy,1,2 Jens Knauer,1 and Reinhard K. Straubinger1,2*

Institute of Immunology, College of Veterinary Medicine,1 Biotechnological-Biomedical Center (BBZ), University of Leipzig, Leipzig, Germany2

Received 22 February 2005/ Returned for modification 11 April 2005/ Accepted 19 May 2005

Lyme borreliosis caused by Borrelia burgdorferi is a persistent infection capable of withstanding the host's vigorous immune response. Several reports have shown that the spirochete's linear plasmids 25 and 28-1 are essential for its infectivity. In this context, it was proposed that Borrelia burgdorferi organisms control their uptake by macrophages and polymorphonuclear leukocytes (PMNs) through plasmid-encoded proteins and that this mechanism confers resistance to phagocytosis. To investigate this proposal, a precise flow-cytometry-based method with human blood was used to study the impact of the plasmids 25 and 28-1 on B. burgdorferi clearance over 150 min and to investigate whether low-passage organisms are more resistant to phagocytosis than high-passage B. burgdorferi. Exposure of human blood PMNs or blood monocytes to fluorescein isothiocyanate-labeled B. burgdorferi B31 organisms lacking the linear plasmids 25, 28-1, or both revealed that all spirochete populations were internalized at the same rate as the wild-type borrelia parent strain B31. Moreover, no differences in phagocytosis kinetics were detected when low- or high-passage wild-type B. burgdorferi B31 or N40 were cocultured with blood cells. Plasmid loss and probable associated surface protein changes due to serial in vitro propagation of B. burgdorferi do not affect the resistance of these organisms to internalization by phagocytic cells. In particular, we found no evidence for a plasmid-controlled (lp25 and lp28-1) resistance of B. burgdorferi to phagocytosis by leukocytes of the host's innate immune system.

* Corresponding author. Mailing address: University of Leipzig, College of Veterinary Medicine, Institute of Immunology, An den Tierkliniken 11, 04103 Leipzig, Germany. Phone: 49-341-9737837. Fax: 49-341-9738147. E-mail: straubinger{at}vetmed.uni-leipzig.de.

Editor: D. L. Burns

Infection and Immunity, September 2005, p. 5547-5553, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5547-5553.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





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