Inan, SerhatBabakurban, Seda TurkogluErbek, Selim SermedTerzi, Yunus KasimSahin, Feride Iffet2021-06-212021-06-2120200250-4685http://hdl.handle.net/11727/6137Background: Adenoid hypertrophy (AH) is one of the possible causes of chronic inflammation in the middle ear. It has been suggested that CX3CL1 and its specific receptor (CX3CR1) could be related with the pathogenesis of some inflammatory diseases. The aim of the present study was to evaluate the role of CX3CL1 and CX3CR1 in the pathogenesis of AH with chronic otitis media with effusion (COME) in children. Materials and methods: Adenoid tissue samples were obtained from 91 pediatric patients and divided into two groups: adenoidectomy only for AH (n: 47) and adenoidectomy in conjunction with ventilation tube insertion for AH + COME (n: 44). Expression levels of CX3CL1 and CX3CR1 genes were compared. Results: Expression levels of CX3CL1 and CX3CR1 in hypertrophic adenoid tissue were not significantly different between the AH + COME and All only groups. Although no significant difference was detected in the expression of CX3CL1 in the adenoid samples, the expression of CX3CR1 was higher in children older than 48 months. Conclusions: When allergy, atopy and chronic adenoiditis does not exist to obstructive adenoid hypertrophy, inflammatory fractalkine chemokine expression levels in adenoid tissue was not observed to be increased in children with COME.enginfo:eu-repo/semantics/closedAccessChronic otitis media with effusionAdenoid hypertrophiaFractalkineCX3CL1CX3CR1article45144500005257361000062-s2.0-85083118199