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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #262463
Title: Innate immune responses to pathogens involved in the porcine respiratory disease complex

Author
item Brockmeier, Susan
item Loving, Crystal
item Baker, Amy

Submitted to: Keystone Symposia
Publication Type: Abstract Only
Publication Acceptance Date: 12/27/2010
Publication Date: 2/26/2011
Citation: Brockmeier, S.L., Loving, C.L., Vincent, A.L. 2011. Innate immune responses to pathogens involved in the porcine respiratory disease complex [abstract]. Keystone Symposia, Immunity in the Respiratory Tract. Poster No. 114. p. 149.

Interpretive Summary:

Technical Abstract: The porcine respiratory disease complex is a multifactorial disease complex caused by a combination of viral and bacterial infectious agents. The list of infectious agents that cause respiratory disease in swine is extensive and includes both viral agents, such as porcine reproductive and respiratory syndrome virus, swine influenza virus (SIV), and porcine respiratory coronavirus; and bacterial agents, such as Bordetella bronchiseptica, Haemophilus parasuis, Mycoplasma hyopneumoniae, and Streptococcus suis. Pigs are a natural host for influenza A virus, and suffer a similar clinical disease to that observed in humans. Although influenza is typically a self-limited infection characterized by high morbidity and low mortality, secondary complications substantially increase flu-associated illness in both pigs and humans. Upon infection, the innate immune response is critical for controlling pathogen spread and initiating the adaptive immune response. Host cells recognize conserved motifs expressed by various pathogens and respond with the production of proinflammatory cytokines. Coinfection can trigger multiple pathways sometimes with altered effects compared to what is seen with each pathogen alone. The effects of both simultaneous coinfection with SIV and B. bronchiseptica and prior infection with SIV on subsequent infection with H. parasuis were studied. Our data indicate that coinfection does not alter the course of influenza disease, but coinfection does increase B. bronchiseptica colonization and persistence in the lower respiratory tract. In addition, pulmonary lesions were exacerbated in coinfected pigs when compared to pigs infected with either agent alone. The pulmonary proinflammatory response in coinfected animals was also heightened, likely contributing to the enhanced pathology. Prior infection with SIV also had an effect on subsequent infection with H. parasuis. Pigs infected with SIV 5-days prior to infection with H. parasuis had increased bacterial colonization of the lung and increased proinflammatory responses. Also, alveolar macrophages collected from pigs infected with SIV 5 days previously exhibited dysregulated innate immune responses to secondary H. parasuis exposure in vitro, providing additional evidence that SIV infection alters host responses to secondary stimulation. Understanding the pathogenesis and immune response to coinfections is critical for developing methods to treat and prevent respiratory disease.