Transcriptional and Pathological Host Responses to Coinfection with Virulent or Attenuated Mycoplasma gallisepticum and Low-Pathogenic Avian Influenza A Virus in Chickens

J A Canter; E R Tulman; J Beaudet; D-H Lee; M May; S M Szczepanek; S J Geary

doi:10.1128/IAI.00607-19

Transcriptional and Pathological Host Responses to Coinfection with Virulent or Attenuated Mycoplasma gallisepticum and Low-Pathogenic Avian Influenza A Virus in Chickens

Infect Immun. 2019 Dec 17;88(1):e00607-19. doi: 10.1128/IAI.00607-19. Print 2019 Dec 17.

Authors

J A Canter¹, E R Tulman¹, J Beaudet^{1

2}, D-H Lee¹, M May³, S M Szczepanek¹, S J Geary⁴

Affiliations

¹ Department of Pathobiology and Veterinary Science, 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 Science, Center of Excellence for Vaccine Research, University of Connecticut, Storrs, Connecticut, USA steven.geary@uconn.edu.

Abstract

The avian pathogen Mycoplasma gallisepticum, the etiological agent of chronic respiratory disease in chickens, exhibits enhanced pathogenesis in the presence of a copathogen such as low-pathogenic avian influenza virus (LPAIV). To further investigate the intricacies of this copathogenesis, chickens were monoinfected or coinfected with either virulent M. gallisepticum strain R_low or LPAIV H3N8 (A/duck/Ukraine/1963), with assessment of tracheal histopathology, pathogen load, and transcriptomic host responses to infection by RNA sequencing. Chickens coinfected with M. gallisepticum R_low followed by LPAIV H3N8 exhibited significantly more severe tracheal lesions and mucosal thickening than chickens infected with LPAIV H3N8 alone and greater viral loads than chickens infected first with H3N8 and subsequently with M. gallisepticum R_low Recovery of live M. gallisepticum was significantly higher in chickens infected first with LPAIV H3N8 and then with M. gallisepticum R_low, compared to chickens given a mock infection followed by M. gallisepticum R_low The transcriptional responses to monoinfection and coinfection with M. gallisepticum and LPAIV highlighted the involvement of differential expression of genes such as Toll-like receptor 15, Toll-like receptor 21, and matrix metallopeptidase 1. Pathway and gene ontology analyses of these differentially expressed genes suggest that coinfection with virulent M. gallisepticum and LPAIV induces decreases in the expression of genes related 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 copathogenesis in the natural host and may contribute to further understanding of copathogen infections of humans and other animals.

Keywords: LPAIV; Mycoplasma gallisepticum; RNA-seq; avian influenza A virus; chicken; immune response.

Publication types

Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

Animals
Bacterial Load
Chickens
Coinfection / pathology*
Gene Expression Profiling
Gene Expression Regulation
Histocytochemistry
Host-Pathogen Interactions
Influenza A virus / growth & development
Influenza in Birds / complications
Influenza in Birds / pathology*
Mycoplasma Infections / complications
Mycoplasma Infections / pathology*
Mycoplasma gallisepticum / growth & development
Poultry Diseases / pathology*
Trachea / pathology*
Viral Load