E-cadherin, Passive Smoking and Allergen Sensitization in Children with Adenoid Hypertrophy
Monday, March 5, 2018
South Hall A2 (Convention Center)
Milos Jesenak, Barbora Uhliarova, Gabriela Bugova, Peter Banovcin, Eva Babusikova
RATIONALE: Adenoid hypertrophy (AH) represents a common problem in children associated with many complications. It was suggested, that allergic sensitization and immune dysregulation could contribute to AH development.

METHODS: In a group of 97 children undergoing adenoidectomy (AT), we analyzed the contribution of allergic sensitization and passive smoking to the development of AH and to the changes of musocal microbiome. We evaluated the concentration of E-cadherin (measured by standard human ELISA E-cadherin kit), a mediator of immunological functions of airway epithelium, in relationship to the surgery and allergic background (evaluated by skin prick tests).

RESULTS: Atopy was confirmed in 83% of children and the most prevalent allergens were house dust mites (HDM) and animal dander. Passive smoking was detected in 37% of children assessed by the questionnaires. In the whole group, no changes in E-cadherin levels before and after the surgery were detected. However, in children exposed to passive smoking, E-cadherin significantly increased after the AT (5393±372 ng/mL vs. 6727±427 ng/mL, p=0.034) and was higher compared to children without exposure to passive smoking (p=0,039). Children sensitized to HDM allergens yielded higher concentration of E-cadherin before and after the surgery compared to non-sensitized (before AT: 7248±599 vs. 5302±387 ng/mL, p =0.028; after AT: 6446±513 vs. 5722±419 ng/mL, p=0.045). Children allergic to Alternaria had higher E-cadherin after AT (7294±906 vs. 5607±336 ng/mL, p=0.049).

CONCLUSIONS: Passive smoking and sensitization to perennial allergens damage and modify the immunological functions of airways epithelium and could contribute to the development of adenoid hypertrophy.