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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
Abstract:
Human parotid saliva contains agglutinins which bind to the surface of streptococci and induce the formation of bacterial aggregates. Bacterial aggregation can be blocked by proteins released from viable PMNs and platelets or by sonic extracts prepared from these cells. PMN and platelet inhibitors display characteristic differences in molecular weight, protease, and temperature sensitivity. The mechanism of action of the inhibitors appears to involve a direct interaction with the salivary agglutinins rather than with the bacteria. It is thus possible that PMN and platelet-derived products might modulate saliva-mediated bacterial aggregation and thereby influence the course of infections in the oral cavity.
Insights
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.
