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Methods for Rapid Transfer and Localization of Lyme Disease Pathogens Within the Tick Gut
Published on: February 15, 2011
Diverse Lyme disease spirochetes bind integrin alpha IIb beta 3 on human platelets
J Coburn1, S W Barthold, J M Leong
1Division of Rheumatology and Immunology, Tufts-New England Medical Center, Boston, Massachusetts 02111.
Infection and Immunity
|December 1, 1994
Summary
Infectious Lyme disease spirochetes bind to human platelets via integrin alpha IIb beta 3. This widespread binding among Borrelia species suggests a role in Lyme disease transmission and pathogenesis.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Lyme disease is a multisystemic infection caused by Borrelia burgdorferi.
- Previous studies indicated infectious Borrelia burgdorferi binds to human platelets through integrin alpha IIb beta 3.
Purpose of the Study:
- To investigate the platelet- and alpha IIb beta 3-binding activity of diverse Lyme disease spirochete strains.
- To determine if this binding is conserved across different Borrelia species that cause Lyme disease.
Main Methods:
- Tested 11 infectious strains of Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii for platelet binding.
- Utilized microtiter wells and suspension assays to assess binding.
- Employed blocking anti-alpha IIb beta 3 antibodies and purified alpha IIb beta 3 to confirm specificity.
- Assessed expression of outer surface proteins OspA, OspB, and OspC via immunoblotting.
Main Results:
- All 11 infectious Borrelia strains demonstrated binding to human platelets.
- Binding was specifically mediated by integrin alpha IIb beta 3.
- Non-infectious strains lacked alpha IIb beta 3 and platelet-binding activity.
- No correlation was found between platelet binding and OspA, OspB, or OspC expression.
Conclusions:
- Integrin alpha IIb beta 3-binding activity is a common characteristic of Borrelia species responsible for Lyme disease.
- This binding is strongly associated with infectivity.
- The findings support a significant role for alpha IIb beta 3 interaction in the transmission and/or pathogenesis of Lyme disease.
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