Thromb Haemost 2006; 95(02): 288-293
DOI: 10.1160/TH05-07-0491
Wound Healing and Inflammation/Infection
Schattauer GmbH

A role for immunoglobulin G in donor-specific Streptococcus sanguis-induced platelet aggregation

Archibald McNicol
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
2   Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada
,
Raymond Zhu
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
,
Robert Pesun
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
,
Caroline Pampolina
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
,
Elke C. Jackson
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
,
George H. W. Bowden
1   Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada
3   Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada
,
Teresa Zelinski
4   Pediatrics & Child Health and Biochemistry, University of Manitoba, Winnipeg, Manitoba, Canada
5   Medical Genetics, University of Manitoba, Winnipeg, Manitoba, Canada
› Author Affiliations
Financial support: Funded by grants from the Canadian Institutes of Health Research to AMcN and from the Winnipeg Rh Institute Foundation to TZ.
Further Information

Publication History

Received 12 July 2005

Accepted after resubmission 09 January 2005

Publication Date:
28 November 2017 (online)

Summary

There is increasing evidence fora relationship between bacterial infections and several cardiovascular disorders. Although the precise mechanism(s) underlying this association is unknown, the direct activation of platelets by bacteria is one possibility. Individual strains of S. sanguis activate platelets in a non-uniform, donor-dependent manner. In the current study, platelet aggregation profiles were obtained for fourteen donors in response to four strains of S. sanguis (2017–78, 133–79, SK112, SK108a) and one of S. gordonii (SK8). The platelets from all donors responded to strains 2017–78 and 133–79,whereas strains SK112, SK8 and SK108a caused aggregation in one, five and twelve donors, respectively. Immunoglobulin G (IgG) binding to strains 2017–78, 133–79 and SK108a were significantly greater than to strains SK112 and SK8. Absorption of IgG by strain 2017–78 caused significant decreases in IgG binding, and platelet aggregation in response, to all strains. Single-strand conformational polymorphisms were observed in the FcγRIIA gene from four donors. Sequencing revealed two known and two novel point mutations, none of which correlated with the aggregation profile. Thus, platelet activation to the various strains depends ona common IgG and, while in most cases the level of IgG binding to S. sanguis determines platelet responsiveness, neither the levels of IgG nor FcγRIIA polymorphisms can fully account for donor variability.

 
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