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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Modulation of bacterial aggregation by PMN and platelet extracts
Inflammation
|June 1, 1983
Summary
Human saliva agglutinins cause streptococcal aggregation. Proteins from neutrophils (PMNs) and platelets block this, suggesting a role in oral cavity infections.
Area of Science:
- Oral microbiology
- Immunology
- Biochemistry
Background:
- Human parotid saliva contains agglutinins that bind to streptococci, promoting bacterial aggregation.
- Bacterial aggregation in the oral cavity can influence the course of infections.
Purpose of the Study:
- To investigate the role of polymorphonuclear leukocytes (PMNs) and platelets in modulating saliva-mediated bacterial aggregation.
- To characterize the inhibitors released by PMNs and platelets.
Main Methods:
- Analysis of proteins released from viable PMNs and platelets, and sonic extracts from these cells.
- Assessment of bacterial aggregation inhibition.
- Characterization of inhibitor properties including molecular weight, protease sensitivity, and temperature sensitivity.
Main Results:
- Proteins from viable PMNs and platelets, or their sonic extracts, effectively blocked streptococcal aggregation induced by salivary agglutinins.
- PMN and platelet inhibitors exhibited distinct characteristics in molecular weight, protease sensitivity, and temperature stability.
- Inhibitor action appeared to target salivary agglutinins directly, not the bacteria.
Conclusions:
- Polymorphonuclear leukocytes (PMNs) and platelets produce products that inhibit saliva-mediated bacterial aggregation.
- These PMN and platelet-derived inhibitors interact with salivary agglutinins.
- Such interactions suggest a mechanism by which PMN and platelet products may modulate oral infections.
