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Pneumococcal immune adherence to human erythrocytes.
J-M Hament1, H van Dijk, A Fleer
1Department of Paediatric Infectious Diseases, Wilhelmina Children's Hospital, University Medical Centre, Utrecht, The Netherlands.
European Journal of Clinical Investigation
|February 18, 2003
Summary
Human red blood cells bind to C3b-coated pneumococci via complement receptor 1, involving both innate and adaptive immunity. Factor I facilitates bacterial detachment, supporting the immune adherence hypothesis.
Area of Science:
- Immunology
- Microbiology
- Hematology
Background:
- Human red blood cells (RBCs) bind C3b-coated microbes via the C3b/CR1 receptor, a process known as immune adherence.
- Pneumococcal adherence to RBCs is crucial for understanding bacterial clearance mechanisms.
Purpose of the Study:
- To quantify pneumococcal adherence to human RBCs using flow cytometry.
- To investigate the kinetics and immune factors involved in pneumococcal-RBC binding.
Main Methods:
- Quantification of pneumococcal adherence to human erythrocytes using Fluorescence-Activated Cell Sorting (FACS) analysis.
- Assessment of the roles of antibodies and complement activation in the binding process.
Main Results:
- Pneumococci bind to human RBCs in the presence of human serum, requiring C3b/C4b coating.
- Complement receptor 1 (CR1) on erythrocytes is the primary ligand for pneumococcal adherence.
- Both mannose-binding lectin (innate immunity) and IgG antibodies (adaptive immunity) contribute to C3b-coated pneumococcal binding.
- Factor I induces detachment of bound pneumococci from RBCs.
Conclusions:
- Pneumococci adhere to RBCs, mediated by C3b coating and CR1.
- Both classical and lectin complement pathways are vital for optimal pneumococcal C3b-coating and subsequent immune adherence.
- Factor I-mediated detachment of pneumococci from RBCs supports the immune adherence hypothesis, targeting bacteria to the spleen.