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Cytolytic complement activity in otitis media with effusion
1Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Finland.
Abstract:
Otitis media with effusion (OME) is a chronic inflammation persisting in the middle ear cavity of at least 8 weeks duration. Middle ear effusion (MEE; n = 38), samples from children suffering from OME were investigated for their direct cytolytic activity or an ability to enhance complement lysis of unsensitized bystander cells. Thirteen of the 38 MEEs had direct endogenous haemolytic activity and 27 samples had an ability to enhance serum-initiated lysis. Using an enzyme immunoassay, high levels of terminal complement complexes (TCC) were detected in the MEE samples (mean 34.1 microg/ml, range 5--89 microg/ml). This indicated strong local complement activation that had progressed to the terminal stage. As one potential factor promoting complement activation we identified both monomeric and trimeric properdin in MEE by Western blotting. By stabilizing C3 and C5 convertases properdin accelerates the alternative and terminal pathways of complement. On the other hand, the membrane attack complex (MAC) inhibitor CD59, which was found to be extensively shed into the MEE in a functionally active form, may control excessive cytotoxicity of the MEE. In conclusion, intense complement activation, up to the terminal level, maintains ongoing inflammation in the middle ear cavity and can pose a threat to the local epithelium.
Insights
Otitis media with effusion involves chronic middle ear inflammation. Complement activation, particularly the terminal complement complexes, plays a key role in this inflammatory process.
Area of Science:
- Immunology
- Otolaryngology
- Molecular Biology
Background:
- Otitis media with effusion (OME) is a persistent middle ear inflammation.
- Middle ear effusion (MEE) samples from children with OME were analyzed.
Purpose of the Study:
- To investigate the role of complement system activation in OME pathogenesis.
- To identify factors contributing to complement activation and regulation in MEE.
Main Methods:
- Analysis of cytolytic activity and complement-mediated lysis in MEE samples.
- Enzyme immunoassay to detect terminal complement complexes (TCC).
- Western blotting to identify properdin and CD59 in MEE.
Main Results:
- Thirteen of 38 MEE samples showed direct hemolytic activity; 27 enhanced serum-initiated lysis.
- High levels of TCC (mean 34.1 microg/ml) indicated terminal complement activation.
- Properdin was identified in MEE, potentially promoting complement activation.
- Active CD59 was detected, possibly regulating cytotoxicity.
Conclusions:
- Intense complement activation, including terminal pathways, sustains middle ear inflammation in OME.
- Properdin may accelerate complement pathways, while CD59 might regulate local cytotoxicity.
- Complement activation poses a threat to the middle ear epithelium in OME.