Friday, June 17, 2011

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

This one is from Steere and company... check it out.

Source link: http://www.ncbi.nlm.nih.gov/pubmed/21641395

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 Jun;178(6):2726-39.

Division of Rheumatology, Allergy and Immunology, the Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.

Abstract

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.

Comments for the moment:

Evidence is emerging? No, actually, this is old news. Dr. Ben Luft and others already knew that genotypes of Bb had differential pathogenicity. Symptom presentation and severity of disease can vary greatly - this is part of the conundrum with Lyme disease.

In terms of mentioning inflammatory response, one thing I want to tease out is the relationship between spirochetal load and inflammatory response versus pathogenicity of genotype and inflammatory response.

In addition to this, on an unrelated note, it would be good to know if particular genotypes are more likely to spend more time in intracellular space and if persister cells contribute to relapsing, chronic infection.

More about this later...

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