In the present study, the main focus was investigating the role of microRNA (miRNA)-302e in infantile pneumonia (IP) and exploring the potential protective mechanisms. Briefly, the expression of miRNA-302e was reduced in a mouse model of IP. In addition, the administration of anti-miRNA-302e increased inflammation and induced the protein expression of RelA, bromodomain-containing protein 4 (BRD4) and nuclear factor (NF)-κB in the
in vitro
model of IP. In contrast, over-expression of miRNA-302e reduced inflammation and suppressed the protein expression of RelA, BRD4 and NF-κB in an
in vitro
model of IP. Small interfering (si)-RelA attenuated the effects of miRNA-302e on inflammation in an
in vitro
model of IP. Consistently, si-BRD4 or si-NF-κB attenuated the effects of miRNA-302e on inflammation in an
in vitro
model of IP. Taken together, the results of the present study demonstrated that miRNA-302e attenuated inflammation in IP through the RelA/ BRD4/ NF-κB signaling pathway.