Down‐regulation of anti‐inflammatory TIPE2 may aggravate adenoidal hypertrophy in children

Adenoidal hypertrophy (AH) is a common disorder in the pediatric population, with common symptoms including mouth breathing, nasal congestion, hyponasal speech, snoring and obstructive sleep apnea. Although the pathogenesis of AH has not been fully elucidated, recent studies have indicated that immune responses may play an important role in AH. Tumor necrosis factor‐alpha (TNF‐α)‐induced protein‐8 like‐2 (TIPE2) is a newly identified protein that negatively regulates the activation of inflammatory pathways. Here, we investigated the effect of TIPE2 in AH in children. We observed that the levels of TNF‐α and interleukin‐6 were greater in the adenoid tissue of AH children than in healthy control subjects (P < 0.01), and this increase was positively correlated with the severity of AH. The level of TIPE2 expression was decreased compared with control and was negatively correlated with AH. TIPE2 overexpression in primary human monocytes (isolated from adenoid tissue of children with AH) inhibited the activation of nuclear factor‐κB and the expression of TNF‐α and interleukin‐6. These results suggest that overexpression of TIPE2 may attenuate AH through inactivation of the nuclear factor‐κB signaling pathway.