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.

Infect Immun. 2005 Sep;73(9):5547-53.

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.

Al-Robaiy S, Knauer J, Straubinger RK.

University of Leipzig, College of Veterinary Medicine, Institute of
Immunology, An den Tierkliniken 11, 04103 Leipzig, Germany.

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.

PMID: 16113271 [PubMed - indexed for MEDLINE]

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