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Complement activation in pediatric patients with recurrent acute otitis media
Yujuan He1, Melissa A Scholes, Gregory J Wiet
1Department of Otolaryngology, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43210, USA.
Insights
Complement activation in the middle ear plays a dual role in recurrent acute otitis media (rAOM). Understanding these pathways can help prevent hearing loss and inflammation in children.
Area of Science:
- Immunology
- Otolaryngology
- Pediatrics
Background:
- Otitis media (OM) is a common childhood illness with unknown roles for complement activation in its development.
- Recurrent acute otitis media (rAOM) can lead to complications like hearing loss.
Purpose of the Study:
- Investigate the beneficial and detrimental roles of complement activation in pediatric rAOM.
- Identify targets for preventing OM sequelae, such as hearing loss.
Main Methods:
- Analyzed middle ear effusion (MEE) and serum from 20 children with rAOM.
- Used ELISA and Western blot to measure complement components (C3a, C5a, sC5-b9) and cytokines (IL-6, IL-8).
- Assessed complement gene expression in human middle ear epithelial cells exposed to otopathogens.
Main Results:
- Demonstrated activation of classical/lectin, alternative, and terminal complement pathways in the middle ear.
- Elevated C3a, C5a, and sC5-b9 levels correlated with longer rAOM episodes (>6 weeks).
- Found a strong correlation between C5a and IL-6/IL-8; otopathogens upregulated complement gene expression in middle ear cells.
Conclusions:
- Complement activation significantly contributes to the inflammatory process in rAOM.
- Targeting specific complement pathways may offer new strategies to prevent inflammatory tissue damage and hearing loss in rAOM.
Objective:
Otitis media (OM) is one of the most common childhood diseases. The relative contribution of complement activation in protection and pathogenesis during OM remains largely unknown. The purpose of this study was to investigate the beneficial and pathogenic contributions of complement activation in the middle ear of pediatric patients with recurrent acute otitis media (rAOM), and therefore to provide a rational approach to prevent sequelae of OM such as hearing loss.
Methods:
Twenty children undergoing pressure equalization tube placement with or without adenoidectomy for rAOM were enrolled in the study. Bacterial cultures, enzyme-linked immunosorbent assay (ELISA) for complement components and cytokines and western blot for complement activation were performed on middle ear effusion (MEE) and serum samples. The levels of complement C3a, C5a and sC5-b9 in MEEs and serum samples were compared. The levels of these factors were also examined in regards to length of episode. Pearson's correlation coefficients were calculated on variables between C5a and IL-6 or IL-8. Complement gene expression in human middle ear epithelial (HMEE) cells induced by otopathogens was evaluated. Data were analyzed with Student's t test or the Mann-Whitney rank sum test. In all cases, a P value of <0.05 was set as the measure of significance.
Results:
Our data demonstrated that the complement classical/lectin, alternative and terminal pathways were activated in the middle ear of children with rAOM. Increased complement components of C3a, C5a and sC5-b9 in MEEs were detected in patients with the episode lasting more than six weeks. There was a strong correlation between C5a and IL-6 or IL-8 in the MEEs. Additionally, otopathogens induced enhanced gene expression of factor B and C3 in HMEE cells, which is beneficial for host defense against invading pathogens.
Conclusion:
Our studies provided important new insights on how complement activation contributes to inflammatory process during rAOM. Knowledge of the activity of the complement pathway in patients with rAOM may stimulate the development of new strategies to prevent middle ear inflammatory tissue destruction by directing treatment to specific pathways within the complement cascade.
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