Allergic airway inflammation is manifested as infiltration of CD4+ T cells and eosinophils in the airway,increased secretion of mucus,airway hyper-reactivity and airway remodeling.IL-25 is a member of the IL-17 family,which can promote and exacerbate Th2 cytokine-mediated airway inflammation after binding to its receptor IL-17RB.The increased IL-25 can induce the secretion of Th2 cytokines,including IL-4,IL-5 and IL-13,which may result in the local infiltration of eosinophils,airway hyperreactivity and therefore the injury of airway.As IL-25 plays an important role in allergic airway inflammation,the present paper would focus on the relationship between IL-25 and allergic airway inflammation.

The respiratory tract is primary contact site of the body and environment,and it is ventilated by 10-20 thousand liters of air per day.Inevitably,the respiratory system comes into contact with airborne microbes,which contain the disease-causing pathogens.Airway epithelial cells (AECs) are known to have innate sensor functions,which are similar to the "professional" immune cells,such as alveolar macrophage and sub-or intra-epithelial dendritic cells (DCs).Thus AECs are able to detect invading microbial danger including different types of respiratory viruses,and mount a potent host response,for example,activating type Ⅰ interferon signaling pathway genes.To avoid chronic inflammation and maintain the immunological homeostasis,the pulmonary system has developed intrinsic mechanisms to control local immune responses.Most recently,the role of AECs in control of local immunity has gained much attention,as 1) AECs express the pattern recognition receptors (PRRs),such as Toll-like receptors,retinoic acid inducible gene Ⅰ (RIG-Ⅰ)-like receptor,and so on,thus AECs are equipped to Participate in innate detection of microbial encounter;2) To keep immunological homeostasis in the respiratory tract,AECs behave not only as innate immune sensors but also as immune modulators in parallel,through modulating the sensitivity of innate immune sensing of both AECs per se and sub-or intra-epithelial immune cells;3) Loss of modularity capacity of AECs might be involved in the development of chronic airway diseases.In present review,how the AECs act will be intensively discussed in response to respiratory viruses and modulate the local immunity through cis-and trans-factors (direct and indirect factors),as well as the consequence of impairment of this control of local immunity,in the development and exacerbation of airway diseases,such as acute and chronic rhinosinusitis.