Porcine coronin 1A contributes to nuclear factor-kappa B (NF-κB) inactivation during Haemophilus parasuis infection.

Abstract

Haemophilus parasuis (H.parasuis) is the etiological agent of porcine polyserositis and arthritis (Glässer's disease) characterized by fibrinous polyserositis, meningitis and polyarthritis, causing severe economic losses to the swine industry. Currently, the molecular basis of this infection is largely unkonwn. Coronin 1A (Coro1A) plays important roles in host against bacterial infection, yet little is known about porcine Coro1A. In this study, we investigated the molecular characterization of porcine Coro1A, revealing that porcine Coro1A was widely expressed in different tissues. Coro1A could be induced by lipopolysaccharide (LPS), polyinosinic acid-polycytidylic acid [poly (I:C)] and H.parasuis in porcine kidney-15 (PK-15) cells. Functional analyses revealed that porcine Coro1A suppressed the NF-κB activation during H.parasuis infection by inhibiting the degradation of IκBα and nuclear translocation of p65. Overexpression of porcine Coro1A inhibited the transcription of NF-κB-mediated downstream genes [Interleukin-6 (IL-6), Interleukin-8 (IL-8) and COX-2] through down-regulation of NF-κB. The results indicated that porcine Coro1A is an important immunity related gene that helps to inhibit NF-kB activation during H. parasuis infection.