tetano
Editor, Senior Moderator
Infect Immun. 2019 Oct 7. pii: IAI.00607-19. doi: 10.1128/IAI.00607-19. [Epub ahead of print] [h=1]Transcriptional and pathological host responses to co-infection with virulent or attenuated Mycoplasma gallisepticum and low pathogenic avian influenza A virus in chickens.[/h]
Canter JA[SUP]1[/SUP], Tulman ER[SUP]1[/SUP], Beaudet J[SUP]1,[/SUP][SUP]2[/SUP], Lee D[SUP]1[/SUP], May M[SUP]3[/SUP], Szczepanek SM[SUP]1[/SUP], Geary SJ[SUP]4[/SUP].
[h=3]Author information[/h] 1 Department of Pathobiology and Veterinary Sciences and the Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut, USA. 2 Department of Allied Health Sciences, University of Connecticut, Storrs, Connecticut, USA. 3 Department of Biomedical Sciences, University of New England College of Medicine, Biddeford, Maine, USA. 4 Department of Pathobiology and Veterinary Sciences and the Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut, USA steven.geary@uconn.edu.
[h=3]Abstract[/h] The avian pathogen Mycoplasma gallisepticum, the etiologic agent of chronic respiratory disease in chickens, exhibits enhanced pathogenesis in the presence of a co-pathogen such as low-pathogenic avian influenza virus (LPAIV). To further investigate the intricacies of this co-pathogenesis, chickens were mono- or co-infected with either virulent M. gallisepticum strain R[SUB]low[/SUB], or LPAIV H3N8 (A/duck/Ukraine/1963) and assessed for tracheal histopathology, pathogen load, and transcriptomic host response to infection using RNA-sequencing. Chickens co-infected with M. gallisepticum R[SUB]low[/SUB] followed by LPAIV H3N8 exhibited significantly more severe tracheal lesions and mucosal thickening than chickens infected with LPAIV H3N8 alone and higher viral loads than chickens infected first with H3N8 and subsequently with M. gallisepticum R[SUB]low[/SUB] Recovery of live M. gallisepticum was significantly higher in chickens infected first with LPAIV H3N8 followed by M. gallisepticum R[SUB]low[/SUB] compared to chickens given a mock infection followed by M. gallisepticum R[SUB]low[/SUB] The transcriptional response to mono- and co-infection with M. gallisepticum and LPAIV highlighted the involvement of differential expression of genes such as TLR15, TLR21, and MMP1. Pathway and gene ontology analysis of these differentially expressed genes suggests that co-infection with virulent M. gallisepticum and LPAIV induces a decrease in expression of genes relating to ciliary activity in vivo and alters multiple immune-related signaling cascades. These data aid in the understanding of the relationship between M. gallisepticum and LPAIV during co-pathogenesis in the natural host and may contribute to the further understanding of co-pathogen infections of humans and other animals.
Copyright ? 2019 American Society for Microbiology.
PMID: 31591166 DOI: 10.1128/IAI.00607-19
Canter JA[SUP]1[/SUP], Tulman ER[SUP]1[/SUP], Beaudet J[SUP]1,[/SUP][SUP]2[/SUP], Lee D[SUP]1[/SUP], May M[SUP]3[/SUP], Szczepanek SM[SUP]1[/SUP], Geary SJ[SUP]4[/SUP].
[h=3]Author information[/h] 1 Department of Pathobiology and Veterinary Sciences and the Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut, USA. 2 Department of Allied Health Sciences, University of Connecticut, Storrs, Connecticut, USA. 3 Department of Biomedical Sciences, University of New England College of Medicine, Biddeford, Maine, USA. 4 Department of Pathobiology and Veterinary Sciences and the Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut, USA steven.geary@uconn.edu.
[h=3]Abstract[/h] The avian pathogen Mycoplasma gallisepticum, the etiologic agent of chronic respiratory disease in chickens, exhibits enhanced pathogenesis in the presence of a co-pathogen such as low-pathogenic avian influenza virus (LPAIV). To further investigate the intricacies of this co-pathogenesis, chickens were mono- or co-infected with either virulent M. gallisepticum strain R[SUB]low[/SUB], or LPAIV H3N8 (A/duck/Ukraine/1963) and assessed for tracheal histopathology, pathogen load, and transcriptomic host response to infection using RNA-sequencing. Chickens co-infected with M. gallisepticum R[SUB]low[/SUB] followed by LPAIV H3N8 exhibited significantly more severe tracheal lesions and mucosal thickening than chickens infected with LPAIV H3N8 alone and higher viral loads than chickens infected first with H3N8 and subsequently with M. gallisepticum R[SUB]low[/SUB] Recovery of live M. gallisepticum was significantly higher in chickens infected first with LPAIV H3N8 followed by M. gallisepticum R[SUB]low[/SUB] compared to chickens given a mock infection followed by M. gallisepticum R[SUB]low[/SUB] The transcriptional response to mono- and co-infection with M. gallisepticum and LPAIV highlighted the involvement of differential expression of genes such as TLR15, TLR21, and MMP1. Pathway and gene ontology analysis of these differentially expressed genes suggests that co-infection with virulent M. gallisepticum and LPAIV induces a decrease in expression of genes relating to ciliary activity in vivo and alters multiple immune-related signaling cascades. These data aid in the understanding of the relationship between M. gallisepticum and LPAIV during co-pathogenesis in the natural host and may contribute to the further understanding of co-pathogen infections of humans and other animals.
Copyright ? 2019 American Society for Microbiology.
PMID: 31591166 DOI: 10.1128/IAI.00607-19