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

Qi, Wenxi; Zhu, Rining; Bao, Chuntong; Xiao, Jiameng; Liu, Baijun; Sun, Ming; Feng, Xin; Gu, Jingmin; Yang, Li; Lei, Liancheng

doi:10.1016/j.vetmic.2019.04.028

Cited by 12 publications

(12 citation statements)

References 34 publications

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“…All these mechanisms can operate together for the benefit of the superinfecting bacteria. A typical example of these indirect interactions is provided by PCV2 and swIAV and porcine pathogenic bacteria such as A. pleuropneumoniae [130] and S. suis [96,97,131] where the bacteria benefit from the prior viral infections. However, bacteria can also directly benefit from a previous viral infection as observed in a study demonstrating that Staphylococcus aureus was able to bind viral HA [132].…”

Section: Bacterium-virus and Virus-bacterium Interactionsmentioning

confidence: 99%

Coinfections and their molecular consequences in the porcine respiratory tract

Saadé

Deblanc

Bougon

et al. 2020

Vet Res

158

166

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Understudied, coinfections are more frequent in pig farms than single infections. In pigs, the term "Porcine Respiratory Disease Complex" (PRDC) is often used to describe coinfections involving viruses such as swine Influenza A Virus (swIAV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), and Porcine CircoVirus type 2 (PCV2) as well as bacteria like Actinobacillus pleuropneumoniae, Mycoplasma hyopneumoniae and Bordetella bronchiseptica. The clinical outcome of the various coinfection or superinfection situations is usually assessed in the studies while in most of cases there is no clear elucidation of the fine mechanisms shaping the complex interactions occurring between microorganisms. In this comprehensive review, we aimed at identifying the studies dealing with coinfections or superinfections in the pig respiratory tract and at presenting the interactions between pathogens and, when possible, the mechanisms controlling them. Coinfections and superinfections involving viruses and bacteria were considered while research articles including protozoan and fungi were excluded. We discuss the main limitations complicating the interpretation of coinfection/superinfection studies, and the high potential perspectives in this fascinating research field, which is expecting to gain more and more interest in the next years for the obvious benefit of animal health.

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Section: Bacterium-virus and Virus-bacterium Interactionsmentioning

confidence: 99%

Coinfections and their molecular consequences in the porcine respiratory tract

Saadé

Deblanc

Bougon

et al. 2020

Vet Res

158

166

View full text Add to dashboard Cite

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“…Moreover, PCV2 also suppresses expression of M2-associated genes via regulation of epigenetic histone methylation. Although recent studies indicated that PCV2-mediated expression of canonical inflammatory cytokines and inhibition of ROS production in macrophages contributed to bacterial coinfection ( 10 , 15 ), the underlying mechanisms still remain obscure. Thus, our findings clarified that PCV2 infection deeply altered macrophage function to facilitate bacterial coinfection via a previously unappreciated mechanism by targeting macrophage polarization.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, the ability of M1 macrophages for clearance of bacteria is largely dependent on production of reactive oxygen species (ROS) ( 56 ). Interestingly, recent study suggested that PCV2 infection promoted APP survival during coinfection of PAMs by inhibiting ROS production in vitro and in vivo ( 10 ). This notion was further supported by another study showing that coinfection of PCV2 and Streptococcus suis serotype 2 (SS2) enhances the survival of SS2 in swine tracheal epithelial cells by decreasing ROS production ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

“…For example, influenza virus and bacterial pneumonia combined are among the most deadly infection in human cases (1,(4)(5)(6). Swine viruses such as porcine reproductive and respiratory syndrome virus (PRRSV) or PCV2 infection often predisposes pigs to bacterial coinfection (7)(8)(9)(10)(11)(12). However, how the host immune responses to one pathogen alters the immune response to another infectious agent in host-pathogen interactions remain largely unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Notably, concurrent infections with other swine pathogens are usually seen in most field PCVAD cases, which exacerbates the pathogenesis of diseases (13,(16)(17)(18). The most frequently observed bacteria in PCVAD cases are Actinobacillus pleuropneumoniae (APP), Glaesserella parasuis and Streptococcus suis (9,10,15,19,20). As the smallest virus known to infect mammal, PCV2 has a single-strand circular DNA genome approximately 1.7 kb in size and preferentially targets the swine immune systems.…”

Section: Introductionmentioning

confidence: 99%

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Macrophage Polarization Modulated by Porcine Circovirus Type 2 Facilitates Bacterial Coinfection

Zhang

Yin

et al. 2021

Front. Immunol.

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Polarization of macrophages to different functional states is important for mounting responses against pathogen infections. Macrophages are the major target cells of porcine circovirus type 2 (PCV2), which is the primary causative agent of porcine circovirus–associated disease (PCVAD) leading to immense economic losses in the global swine industry. Clinically, PCV2 is often found to increase risk of other pathogenic infections yet the underlying mechanisms remain to be elusive. Here we found that PCV2 infection skewed macrophages toward a M1 status through reprogramming expression of a subset of M1-associated genes and M2-associated genes. Mechanistically, induction of M1-associated genes by PCV2 infection is dependent on activation of nuclear factor kappa B (NF-κB) and c-jun N-terminal kinase (JNK) signaling pathways whereas suppression of M2-associated genes by PCV2 is via inhibiting expression of jumonji domain containing-3 (JMJD3), a histone 3 Lys27 (H3K27) demethylase that regulates M2 activation of macrophages. Finally, we identified that PCV2 capsid protein (Cap) directly inhibits JMJD3 transcription to restrain expression of interferon regulatory factor (IRF4) that controls M2 macrophage polarization. Consequently, sustained infection of PCV2 facilitates bacterial infection in vitro. In summary, these findings showed that PCV2 infection functionally modulated M1 macrophage polarization via targeting canonical signals and epigenetic histone modification, which contributes to bacterial coinfection and virial pathogenesis.

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