title: Influenza virus coinfection with Bordetella bronchiseptica enhances bacterial colonization and host responses exacerbating pulmonary lesions.
abstract: Influenza virus (Flu) infection and secondary complications are a leading cause of morbidity and mortality worldwide. The increasing number of annual Flu cases, coupled with the recent Flu pandemic, has amplified concerns about the impact of Flu on human and animal health. Similar to humans, Flu is problematic in pigs, not only as a primary pathogen but as an agent in polymicrobial pneumonia. Bordetella species play a role in mixed infections and often colonize the respiratory tract without overt clinical signs. Pigs serve as a valuable animal model for several respiratory pathogens, including Bordetella (Bb) and Flu. To investigate Flu/Bb coinfection pathogenesis, a study was completed in which pigs were inoculated with Flu-only, Bb-only or both agents (Flu/Bb). Results indicate that Flu clearance is not altered by Bb infection, but Flu does enhance Bb colonization. Pulmonary lesions in the Flu/Bb group were more severe when compared to Flu-only or Bb-only groups and Bb did not cause significant lesions unless pigs were coinfected with Flu. The type I interferon response was elevated in coinfected pigs, but increased expression of antiviral genes Mx and PKR did not appear to enhance Flu clearance in coinfected pigs, as viral clearance was similar between Flu/Bb and Flu-only groups. IL-1beta and IL-8 were elevated in lungs of coinfected pigs, correlating to the days enhanced lesions were observed. Overall, Flu infection increased Bb colonization and enhanced production of proinflammatory mediators that likely contribute to exacerbated pulmonary lesions.
authors.affiliation: Respiratory Diseases of Livestock Research Unit, USDA, Agricultural Research Service, National Animal Disease Center, Ames, IA 50010, USA. crystal.loving@ars.usda.gov
authors.forename: Crystal L
authors.initials: CL
authors.lastname: Loving
authors.forename: Susan L
authors.initials: SL
authors.lastname: Brockmeier
authors.forename: Amy L
authors.initials: AL
authors.lastname: Vincent
authors.forename: Mitchell V
authors.initials: MV
authors.lastname: Palmer
authors.forename: Randy E
authors.initials: RE
authors.lastname: Sacco
authors.forename: Tracy L
authors.initials: TL
authors.lastname: Nicholson
mesh_terms: D000818:Animals; D001885:Bordetella Infections / Q000150:complications* / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D016950:Bordetella bronchiseptica / Q000276:immunology / Q000472:pathogenicity; D004195:Disease Models, Animal; D005260:Female; D019204:GTP-Binding Proteins / Q000096:biosynthesis; D007370:Interferon Type I / Q000096:biosynthesis; D053583:Interleukin-1beta / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D008168:Lung / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D064547:Myxovirus Resistance Proteins; D009975:Orthomyxoviridae / Q000276:immunology / Q000472:pathogenicity; D009976:Orthomyxoviridae Infections / Q000150:complications* / Q000276:immunology / Q000473:pathology* / Q000821:virology; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology* / Q000821:virology*; D019892:eIF-2 Kinase / Q000096:biosynthesis
chemical_list: D007370:Interferon Type I; D053583:Interleukin-1beta; D016209:Interleukin-8; D064547:Myxovirus Resistance Proteins; D019892:eIF-2 Kinase; D019204:GTP-Binding Proteins