Reduced iNOS expression in adenoids from children with otitis media with effusion


Anna Granath, MD, Division of ENT diseases, Department of Clinical Sciences, Intervention and Technology, Karolinska Institute, Karolinska University Hospital, Huddinge, S-141 86 Stockholm, Sweden
Tel.: +46 8 58580000; +46 733 528014
Fax: +46 8 746 7551


Granath A, Norrby-Teglund A, Uddman R, Cardell L-O. Reduced iNOS expression in adenoids from children with otitis media with effusion.
Pediatr Allergy Immunol 2010: 21: 1151–1156.
© 2010 John Wiley & Sons A/S

Nitric oxide (NO) is a key mediator in the local immune response of human airways. Inducible NO-synthases (iNOS), and endothelial NO-synthases (eNOS) are two enzymes known to regulate its production. The role of NO in middle ear disease is not fully known. Previous studies suggest that NO might have a dual role, both promoting and suppressing middle ear inflammation. The aim of the present study was to compare the eNOS and iNOS expression in adenoids obtained from children with otitis media with effusion (OME) with the expression seen in adenoids derived from children without middle ear disease. In addition, the expression of IL-1β and TNF-α were analyzed, because of their role in the iNOS-induction pathway. The iNOS and eNOS expression were analyzed with real-time PCR in 8 OME and 11 control adenoids. The corresponding proteins were demonstrated by immunohistochemical staining of adenoid tissue. A Luminex® assay was performed to analyze IL-1β and TNF-α in nasopharyngeal secretion in 10 OME and 8 controls, and immunohistochemistry was performed on adenoid tissue and imprints from the adenoid surface. Children with OME exhibited lower levels of iNOS than controls without middle ear disease. No such difference was seen for eNOS. The corresponding proteins were found mainly in conjunction with surface epithelium. No significant changes were seen among the cytokines tested. The present results indicate that local induction of iNOS in adenoids might be of importance for preventing development of OME.