Serine-Rich Repeat Adhesins Mediate Shear-Enhanced Streptococcal Binding to Platelets

Author:

Yakovenko Olga1,Nunez Jamie1,Bensing Barbara23,Yu Hai4,Mount Jonathan1,Zeng Jie45,Hawkins Jasmine1,Chen Xi4,Sullam Paul M.23,Thomas Wendy1ORCID

Affiliation:

1. Department of Bioengineering, University of Washington, Seattle, Washington, USA

2. San Francisco VA Medical Center, San Francisco, California, USA

3. Department of Medicine, University of California, San Francisco, California, USA

4. Department of Chemistry, University of California, Davis, California, USA

5. School of Food Science, Henan Institute of Science and Technology, Xinxiang, China

Abstract

ABSTRACT The binding of bacteria to platelets is thought to be a central event in the pathogenesis of infective endocarditis. The serine-rich repeat (SRR) glycoproteins of viridans group streptococci have been shown to mediate platelet binding in vitro and to contribute to virulence in animal models. However, it is not known whether SRR adhesins can mediate streptococcal binding under the high fluidic shear stress conditions present on the endocardial surface. We found that three streptococcal SRR adhesins (GspB, Hsa, and SrpA) with differing structures and sialoglycan binding specificities nevertheless exhibited similar biomechanical properties. All three adhesins mediated shear-enhanced streptococcal binding to immobilized platelets through the platelet receptor GPIbα. Shear-enhanced adhesion was manifested in three ways. First, the number of circulating streptococci binding via SRR adhesins to immobilized platelet receptors peaked at 1 dyn/cm 2 . Second, bound streptococci switched from weak rolling to strong stationary adhesion as shear stress increased to 10 dyn/cm 2 . Third, while a few streptococci detached each time the flow was increased, the majority of streptococci bound to platelets remained firmly attached through 20 to 80 dyn/cm 2 (shear levels typical of arteries and the endocardium). Thus, all three adhesins mediated shear-enhanced streptococcal binding to platelets under the flow conditions found in heart valves. The ability of the SRR adhesins to mediate shear-enhanced binding strongly suggests that they form catch bonds that are activated by tensile force and provides a mechanism for the selective targeting of bacteria to platelet receptors immobilized on the endocardial surface.

Funder

HHS | NIH | National Institute of Allergy and Infectious Diseases

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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