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Related Experiment Video

Updated: Jun 17, 2026

Introducing Shear Stress in the Study of Bacterial Adhesion

Introducing Shear Stress in the Study of Bacterial Adhesion

Published on: September 2, 2011

Shear-enhanced oral microbial adhesion.

Albert M Ding¹, Robert J Palmer, John O Cisar

¹National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.

Applied and Environmental Microbiology

|December 22, 2009

Summary

This summary is machine-generated.

Shear forces enhance Streptococcus gordonii adhesion to sialic acid receptors, unlike Actinomyces spp. This interaction is crucial for infective endocarditis pathogenesis.

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Area of Science:

Microbiology
Molecular Biology
Pathogenesis

Background:

Oral bacteria like Actinomyces spp. and Streptococcus gordonii cause infections.
Bacterial adhesion to host tissues is a key step in pathogenesis.
Sialic acid-containing receptors are involved in host-pathogen interactions.

Purpose of the Study:

To investigate the role of shear forces in bacterial adhesion.
To compare shear-enhanced adhesion between oral Actinomyces spp. and Streptococcus gordonii.
To understand the mechanism of Streptococcus gordonii adhesion to sialic acid receptors.

Main Methods:

Studying fimbria-mediated adhesion of oral Actinomyces spp.
Analyzing Hsa-mediated adhesion of Streptococcus gordonii to sialic acid-containing receptors under shear conditions.

Main Results:

Shear-enhanced adhesion was observed for Hsa-mediated adhesion of Streptococcus gordonii.
Fimbria-mediated adhesion of oral Actinomyces spp. did not show shear enhancement.
Streptococcus gordonii adhesion to sialic acid receptors is influenced by shear forces.

Conclusions:

Shear forces play a significant role in the adhesion of Streptococcus gordonii via Hsa-mediated interactions.
The mechanism of adhesion differs between oral Actinomyces spp. and Streptococcus gordonii under shear stress.
Understanding shear-enhanced adhesion is important for the pathogenesis of infective endocarditis.