Qiao Pan, Xiumei Wang, Tong Liu, Ying Yu, Lu Li, Rui Zhou, Ganwu Li, Jiuqing Xin

Infect Immun. 2020 Apr 20. pii: IAI.00164-20. doi: 10.1128/IAI.00164-20. [Epub ahead of print]

Abstract

Mycoplasma hyopneumoniae (M. hyopneumoniae) causes the disease porcine enzootic pneumonia, a highly contagious and chronic disease affecting pigs. Understanding the molecular mechanisms of its pathogenicity is critical for developing effective interventions to control this swine respiratory disease. Here, we describe a novel virulence mechanism, by which M. hyopneumoniae interferes with the host unfolded protein response (UPR) and eventually facilitates bacterial adhesion and infection. We observed that M. hyopneumoniae infection suppressed the UPR target molecules GRP78 and CHOP by reducing PERK/eIF2α phosphorylation, ATF6 cleavage and XBP1 splicing. Interestingly, further analyses revealed that host UPR inhibition subsequently suppressed the NF-κB pathway, leading to the reduced production of porcine beta-defensin 2 (PBD-2), thus facilitating M. hyopneumoniae adherence and infection. This study provides new insights into the molecular pathogenesis of M. hyopneumoniae and sheds light upon their interactions with the host.

Copyright © 2020 American Society for Microbiology.