|RAJÃO, DANIELA - Non ARS Employee|
|ABENTE, EUGENIO - Orise Fellow|
|GAUGER, PHILLIP - Iowa State University|
Submitted to: Conference Research Workers Disease Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 11/4/2016
Publication Date: 12/4/2016
Citation: Nicholson, T.L., Vincent, A.L., Brockmeier, S., Rajão, D.S., Abente, E.J., Gauger, P.C. 2016. The B. bronchiseptica type III secretion system does not negatively affect the protective immunity induced by influenza A virus vaccines. Conference of Research Workers in Animals Diseases Meeting. Paper No. P139.
Technical Abstract: B. bronchiseptica is a widely prevalent respiratory bacterial pathogen that infects a variety of wild and domesticated animals, including swine. Infection results in long-term colonization of the upper respiratory tract resulting in a range of clinical outcomes from asymptomatic carriage to lethal pneumonia. B. bronchiseptica expresses many virulence factors, including a type III secretion system (T3SS). The B. bronchiseptica T3SS is required for maximal disease severity and persistence throughout the lower swine respiratory tract. Additionally, the T3SS dampens the adaptive immune response by hindering the development of serum anti-Bordetella antibody levels and inducing an IL-10 response, enabling B. bronchiseptica to persistently colonize the respiratory tract. Influenza A virus (IAV) is an economically important zoonotic pathogen that causes an acute respiratory infection in swine and is considered a public health concern. Vaccination is the main strategy used to control and diminish disease burden. The hemagglutinin (HA) protein is the primary target of protective immune responses and the major component in swine (IAV) vaccines. Given the ability of the B. bronchiseptica T3SS to diminish adaptive immune responses, we hypothesized that T3SS would negatively affect the protective immunity in pigs vaccinated against IAV while concurrently colonized with B. bronchiseptica. To test this hypothesis, pigs were intranasally inoculated with a wild-type B. bronchiseptica strain or a T3SS B. bronchiseptica mutant. After 14 days, pigs were vaccinated against H3N2 as a live-attenuated influenza virus (LAIV) vaccine or as a whole inactivated virus (WIV) vaccine. To maximize the detection of any decrease in vaccine strain efficacy, pigs were subsequently challenged with a H3N2 strain from a separate antigenic cluster. No differences in clinical disease, virus titers, or lung lesions were observed among pigs colonized with wild-type B. bronchiseptica or the T3SS B. bronchiseptica mutant regardless of the vaccine platform used. Our results demonstrate that the B. bronchiseptica T3SS does not negatively affect the protective immunity induced by influenza A virus vaccines.