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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #227007
Title: Investigating the porcine immune reponse to Haemophilus parasuis

Author
item Loving, Crystal
item Brockmeier, Susan
item Baker, Amy
item Nicholson, Tracy
item Register, Karen

Submitted to: Gordon Research Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 5/15/2008
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Haemophilus parasuis is the causative agent of Glässers disease in swine, which is characterized by systemic invasion of the bacteria to serosal surfaces, resulting in inflammation and induction of pleuritis, peritonitis, and arthritis. In addition, certain strains of H. parasuis cause pneumonia when restricted to the respiratory tract. Similar to Haemophilus influenzae in humans, H. parasuis can be isolated from the nose of healthy pigs but the mechanism of transition from carrier state to invasive disease is unknown. There are 15 designated H. parasuis serovars and it has been reported that some are more pathogenic than others, though the relationship between serotype and invasiveness in unclear. As with H. flu, there are also several strains of nontypable H. parasuis that can cause disease. Macrophages are important in host defense and initiation of immune responses after infection, thus we have focused attention on investigating macrophage responses to H. parasuis. Alveolar macrophages (AMac), but not peritoneal macrophages (PMac), had increased mRNA levels of TNF-alpha, IL-1beta and IL-8 regardless of the H. parasuis strain cells were stimulated with. In addition, IL-10 levels were slightly elevated in AMac but not PMac. One-day after in vivo H. parasuis challenge, lung lavage cells had elevated mRNA levels of RANTES and IL-6, but not TNF-alpha or IL-8. This differed from tracheal epithelial cells that had enhanced expression of IL-8 and IL-6 mRNA after challenge. Influenza virus has been shown to enhance susceptibility to secondary bacterial infection, therefore we examined alterations in AMac responses to H. parasuis 21-days after flu-virus infection. Our results show that prior exposure to flu virus results in a dysregulation of AMac responses to H. parasuis, which may help explain the enhanced susceptibility to secondary bacterial pneumonia. Overall, these data indicate that AMac do respond to H. parasuis with the production of proinflammatory mediators and this response can be altered by prior influenza virus infection.