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Saturday, July 23, 2011

[AlternativeAnswers] Borrelia burgdorferi RST1 (OspC Type A) Genotype Is Associated with Greater Inf

 


Borrelia burgdorferi RST1 (OspC Type A) Genotype Is Associated with
Greater Inflammation and More Severe Lyme Disease.

Strle K, Jones KL, Drouin EE, Li X, Steere AC

Am. J. Pathol. 2011 06; 178 (6): 2726-39

Evidence is emerging for differential pathogenicity among Borrelia
burgdorferi genotypes in the United States. By using two linked
genotyping systems, ribosomal RNA intergenic spacer type (RST) and outer
surface protein C (OspC), we studied the inflammatory potential of B.
burgdorferi genotypes in cells and patients with erythema migrans or
Lyme arthritis. When macrophages were stimulated with 10 isolates of
each RST1, RST2, or RST3 strain, RST1 (OspC type A)-stimulated cells
expressed significantly higher levels of IL-6, IL-8, chemokine ligand
(CCL) 3, CCL4, tumor necrosis factor, and IL-1β, factors associated with
innate immune responses. In peripheral blood mononuclear cells, RST1
strains again stimulated significantly higher levels of these mediators.
Moreover, compared with RST2, RST1 isolates induced significantly more
interferon (IFN)-α, IFN-γ, and CXCL10, which are needed for adaptive
immune responses; however, OspC type I (RST3) approached RST1 (OspC type
A) in stimulating these adaptive immune mediators. Similarly, serum
samples from patients with erythema migrans who were infected with the
RST1 genotype had significantly higher levels of almost all of these
mediators, including exceptionally high levels of IFN-γ-inducible
chemokines, CCL2, CXCL9, and CXCL10; and this pronounced inflammatory
response was associated with more symptomatic infection. Differences
among genotypes were not as great in patients with Lyme arthritis, but
those infected with RST1 strains more often had antibiotic-refractory
arthritis. Thus, the B. burgdorferi RST1 (OspC type A) genotype,
followed by the RST3 (OspC type I) genotype, causes greater inflammation
and more severe disease, establishing a link between spirochetal
virulence and host inflammation.

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