Abstract
Streptococcus pneumonia, one of the major colonizers in nasopharyngeal adenoids, has been the predominant pathogen causing acute otitis media (AOM) in children. Recent evidence suggests an association between IL-17A-mediated immune response and the clearance of pneumococcal colonization in nasopharyngeal adenoids. Here, we evaluated the expressions of IL-17A and associated genes in hypertrophic adenoid tissues of children with sleep-disordered breathing (SDB) and otitis media with effusion (OME) and their association with pneumococcal carriage. Sixty-six pediatric patients with adenoid hypertrophy were enrolled. During adenoidectomy, nasopharyngeal swab and adenoid tissues were used to determine pneumococcal carriage and IL-17A expression. Our results revealed significantly higher levels of IL-17A and IL-17A:IL-10 mRNA in the SDB patients positive for nasopharyngeal pneumococcal carriage than those negative. However, these differences were not significant in the OME group. These results suggested, in OME patients, prolonged or chronic pneumococcal carriage may occur because of insufficient IL-17A-mediated mucosal clearance, and could further lead to AOM and OME development.
Highlights
Nasopharyngeal adenoids have been speculated to be associated with otitis media, sinusitis, and obstructive sleep apnea syndrome (OSAS) in children[1,2,3,4]
Bacterial colonization in nasopharyngeal adenoid frequently precedes the onset of some invasive diseases and serves as a reservoir to spread within the community[4,8]
We further evaluated the expressions of IL-17A and associated genes in the hypertrophic adenoid tissue of children with sleep-disordered breathing (SDB) and Otitis media with effusion (OME), and their association with pneumococcal carriage
Summary
Nasopharyngeal adenoids have been speculated to be associated with otitis media, sinusitis, and obstructive sleep apnea syndrome (OSAS) in children[1,2,3,4]. The hypertrophic adenoid tissue causes narrowing of the upper airway as a common etiology of sleep-disordered breathing (SDB) or OSAS in children[3], and represents a reservoir for seeding of pathogens to the middle ear, paranasal sinus, and even the invasive diseases, such as pneumonia, bacteremia, and meningitis[1]. We further evaluated the expressions of IL-17A and associated genes in the hypertrophic adenoid tissue of children with SDB and OME, and their association with pneumococcal carriage
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