Exclusion of IL-21 in the pathogenesis of OVA-induced asthma in mice.

Asthma is characterized by airway inflammation, mucus overproduction, and airway hyperreactivity. Cytokines, especially T helper 2-derived cytokines interleukin (IL)-4, IL-5, and IL-13, are involved in the pathogenesis of asthma. IL-21 has a variety of effects on the immune system. However, the contribution of IL-21 to the development of allergic diseases is currently controversial. The aim of this study was to investigate the effect of IL-21 on asthma airway inflammation in vivo. A murine ovalbumin (OVA)-induced allergic asthma model was used. The concentration of IL-21 in the bronchoalveolar lavage fluid (BALF) of mice was evaluated by enzyme-linked immunosorbent assay. BALF cellularity, lung histopathology, and sera IgE levels were compared between the normal control group, OVA sensitization/challenge group, and OVA sensitization/challenge plus IL-21-administered group. An OVA-induced allergic rhinitis model with IL-21 was used as a positive control and the infiltration of eosinophils in the nasal mucosa was evaluated. The concentration of IL-21 in the BALF was lower in the asthmatic group compared with the normal control group. However, no significant differences in airway eosinophilia, lung histopathology, and sera IgE levels were observed between the OVA sensitization/challenge group and OVA sensitization/challenge plus IL-21-administered group. Decreased eosinophilic infiltration of nasal mucosa was observed in the positive control allergic rhinitis model administered IL-21 during the challenge period. Exogenous administration of IL-21 alone may not alleviate allergic lung inflammation. The role of IL-21 in allergic lung inflammation needs further research.