Piperine inhibits eosinophil infiltration and airway hyperresponsiveness by suppressing T cell activity and Th2 cytokine production in the ovalbumin-induced asthma model

Objectives This study aimed to investigate the effect of piperine on airway hyper‐responsiveness, pulmonary eosinophilic infiltration, various immune cell phenotypes, Th2 cytokine production, immunoglobulin E and histamine production in a murine model of asthma. Methods Asthma was induced in Balb/c mice by ovalbumin sensitization and inhalation. Piperine (4.5 and 2.25 mg/kg) was orally administered 5 times a week for 8 weeks. At 1 day after the last ovalbumin exposure, airway hyperresponsiveness was determined and samples of bronchoalveolar lavage fluid, lung cells and serum were collected for further analysis. Key findings Piperine‐treated groups had suppressed eosinophil infiltration, allergic airway inflammation and airway hyperresponsiveness, and these occurred by suppression of the production of interleukin‐4, interleukin‐5, immunoglobulin E and histamine. Moreover, polymerase chain reaction products for thymus and activation regulated chemokine from lung cell RNA preparations were decreased in the piperine‐treated group compared with control groups, although transforming growth factor‐β products were increased in the piperine‐treated group. Conclusions The results suggest that the therapeutic mechanism by which piperine effectively treats asthma is based on a reduction of Th2 cytokines (interleukin‐4, interleukin‐5), eosinophil infiltration, and by marked reduction of thymus and activation regulated chemokine, eotaxin‐2 and interleukin‐13 mRNA expression (especially transcription of nuclear factor‐β dependent genes) in lung tissue, as well as reduced interleukin‐4, interleukin‐5 and eotaxin levels in bronchoalveolar lavage fluid, and histamine and ovalbumin‐specific immunoglobulin E production in serum.