Newcastle disease (ND), an acute and highly contagious
avian disease caused by virulent Newcastle disease virus (NDV), often results in severe economic losses worldwide every year. Although it is clear that
microRNAs (
miRNAs) are implicated in modulating innate immune response to invading microbial pathogens, their role in host defense against NDV
infection remains largely unknown. Our prior study indicates that gga-miR-19b-3p is up-regulated in NDV-infected DF-1 cells (a chicken embryo fibroblast cell line) and functions to suppress NDV replication. Here we report that overexpression of gga-miR-19b-3p promoted the production of NDV-induced inflammatory
cytokines and suppressed NDV replication, whereas inhibition of endogenous gga-miR-19b-3p expression had an opposite effect. Dual-
luciferase and gene expression array analyses revealed that gga-miR-19b-3p directly targets the mRNAs of ring finger
protein 11 (RNF11) and zinc-finger
protein, MYND-type containing 11 (ZMYND11), two negative regulators of
nuclear factor kappa B (NF-κB) signaling, in DF-1 cells. RNF11 and ZMYND11 silencing by
small interfering RNA (
siRNA) induced NF-κB activity and inflammatory
cytokine production, and suppressed NDV replication; whereas ectopic expression of these two
proteins exhibited an opposite effect. Our study provides evidence that gga-miR-19b-3p activates NF-κB signaling by targeting RNF11 and ZMYND11, and that enhanced inflammatory
cytokine production is likely responsible for the suppression of NDV replication.