Intestinal dysbacteriosis potentiates ovalbumin-induced allergic airway inflammation by inhibiting microRNA-130a to upregulate tumor necrosis factor α.

Allergic airway diseases (AAD), including chronic disorders such as allergic rhinitis, are resulted from complicated immunological interactions. Intestinal dysbacteriosis (ID) has been implicated in immune response to respiratory infections. We aimed to investigate the effect of ID on a mouse model of AAD, and the potential molecular factors involved. Ovalbumin (OVA) was employed to sensitize and challenge mice to elicit allergic inflammation in the upper as well as the lower airways. OVA-induced AAD model mice and control mice were raised with or without antibiotics treatment to establish the combinational AAD + ID mouse model. Characteristic symptoms of AAD were evaluated in regard to allergic symptoms, serum OVA specific IgE level, as well as inflammation cells, cytokines and microRNA expression profile in nasal lavage fluid (NALF) and bronchoalveolar lavage fluid (BALF). In AAD mice, ID caused increased nasal rubbing, sneezing, serum OVA specific IgE level and pro-inflammatory cytokine tumor necrosis factor α (TNF-α) in NALF and BALF. ID also inhibited microRNA-130a of AAD mice. Further molecular experiments indicated that microRNA-130a could specifically target and repress TNF-α. ID increases the susceptibility to AAD and allergic inflammatory response, possibly by inhibiting microRNA-130a to upregulate TNF-α.