Porcine circovirus type 2 promotes Actinobacillus pleuropneumoniae survival during coinfection of porcine alveolar macrophages by inhibiting ROS production.


Journal

Veterinary microbiology
ISSN: 1873-2542
Titre abrégé: Vet Microbiol
Pays: Netherlands
ID NLM: 7705469

Informations de publication

Date de publication:
Jun 2019
Historique:
received: 10 01 2019
revised: 18 04 2019
accepted: 24 04 2019
entrez: 10 6 2019
pubmed: 10 6 2019
medline: 27 6 2019
Statut: ppublish

Résumé

Actinobacillus pleuropneumoniae (APP) and porcine circovirus type 2 (PCV2) are both important pathogens of the porcine respiratory disease complex (PRDC), which results in significant worldwide economic losses. Recently, PCV2 and APP coinfection has been described in the worldwide pork industry, and represents an extremely complex situation in veterinary medicine. However, the mechanism of their coinfection has not been investigated. In this study, we found that PCV2 promoted APP adhesion to and invasion of porcine alveolar macrophages (PAMs) during coinfection. Additionally, PCV2 suppressed reactive oxygen species (ROS) production by inhibiting cytomembrane NADPH oxidase activity, which was beneficial for APP survival in PAMs in vitro. During coinfection, PCV2 weakened the inflammatory response and macrophage antigen presentation by decreasing TNF-α, IFN-γ and IL-4 expression, and reduced clearance of the invading bacteria. The host-cell experimental results were verified in a mouse model. The findings provide a deeper and novel understanding of porcine coinfection, and will be extremely helpful for the design of strategies for PRDC control.

Identifiants

pubmed: 31176418
pii: S0378-1135(19)30041-0
doi: 10.1016/j.vetmic.2019.04.028
pii:
doi:

Substances chimiques

Antibodies, Viral 0
Cytokines 0
Reactive Oxygen Species 0
NADPH Oxidases EC 1.6.3.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

93-101

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Wenxi Qi (W)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Rining Zhu (R)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Chuntong Bao (C)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Jiameng Xiao (J)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Baijun Liu (B)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Ming Sun (M)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Xin Feng (X)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Jingmin Gu (J)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China.

Yang Li (Y)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China. Electronic address: liyang_0317@jlu.edu.cn.

Liancheng Lei (L)

Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis/College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, PR China; College of Animal Science, Yangtze University, Jingzhou, Hubei, 434023, PR China. Electronic address: leiliancheng@163.com.

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Classifications MeSH