Although
atrial natriuretic peptide (
ANP) has been well recognized for its role in the regulation of volume-pressure homeostasis in cardiovascular system, its impact on respiratory system, particularly on the pathogenesis of acute allergic
asthma, is yet to be elucidated. In the present report, we induced mice with OVA for onset of acute allergic
asthma along with the administration of recombinant
ANP or
A71915 (an antagonist for
ANP/
natriuretic peptide receptor A, NPRA). It was noted that treatment of mice with
ANP significantly promoted inflammatory infiltration in the airway and the production of inflammatory
cytokines in the bronchoalveolar lavage fluid (BALF) and lung homogenates, and the number of inflammatory cells in the BALF was significantly higher as compared with that of PBS treated asthmatic mice. Moreover, blockade of
ANP/NPRA signaling by
A71915 almost completely attenuated the effect of
ANP administration. Mechanistic studies revealed that
ANP repressed the expression of Th1
transcription factor T-bet, but enhanced Th2 transcription GATA3 expression. Together, our data provided feasible evidence suggesting that
ANP/NPRA signaling predominantly induces a Th2-type response in favor of
pathological processes during the course of acute allergic
asthma.