Evaluation of cytokines in nasal secretions in children with bronchial asthma and concomitant upper respiratory tract pathology

Background. In children with bronchial asthma (BA), the upper respiratory tract pathology (URT; allergic rhinitis, adenoid hypertrophy) is often observed, which contributes to the uncontrolled BA course. Inflammation in both the upper and lower airways can be uniform, which may aggravate the BA course. However, it is necessary to differentiate the type of inflammation, which can be caused by a Th-2 or Th-1 immune response. Depending on the type of inflammation, further treatment tactics will depend. Therefore, it is important to study the local immunological status in patients with BA and URT pathology.

Objective. Evaluation of the interleukin-4 (IL-4), IL-5, IL-10, IL-8, IL-18, tumor necrosis factor-α (TNF-α) levels in nasal secretions in children with adenoid hypertrophy (AH), allergic rhinitis (AR) and their combination with BA.

Methods. The study involved 107 children aged 4 to 10 years. Group 1 consisted of children diagnosed with BA in combination with AR and AH (n=38); Group 2 (comparison) – children diagnosed with AR (n=32); Group 3 – children with AH (n=25); control group – 12 healthy children. The IL-4, IL-8, IL-18, IL-10, TNF-α levels were determined in nasal secretions using enzyme-linked immunosorbent assay (ELISA) kits from Vector-Best JSC (Russia, Novosibirsk). The IL-5 concentration was determined in nasal secretions by solid-phase ELISA using the IL-5 Human ELISA Kit from Invitrogen Thermo Fisher Scientific (USA). Cytokine concentrations were measured using a Multiscan Fc immunoassay analyzer (Thermo Scientific) and expressed in pg/ml.

Results. In children with BA in combination with AR and AH, a significant increase in the IL-4, IL-5, IL-10 and TNF-α levels was obtained, in children with AR – only IL-4 and IL-5 (p<0.05) .

Conclusion. The allergic process implies the same tendency for the production of cytokines, regardless of the nosological form, and the combination of nosologies leads to more pronounced inflammation. AH does not affect the local cytokine status, however, it contributes to the severity of clinical manifestations.