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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #250667

Title: Prior Swine Influenza Virus Infection Enhances Pulmonary Responses to Secondary Haemophilus parasuis Infection

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

Submitted to: International Pig Veterinary Society (IPVS)
Publication Type: Proceedings
Publication Acceptance Date: 3/30/2010
Publication Date: 7/18/2010
Citation: Loving, C.L., Brockmeier, S., Vincent, A.L. 2010. Prior Swine Influenza Virus Infection Enhances Pulmonary Responses to Secondary Haemophilus parasuis Infection. In: Proceedings of the Pig Veterinary Society International Congress, July 18-21, 2010, Vancouver, Canada. p. 264.

Interpretive Summary:

Technical Abstract: Swine Influenza virus (SIV) infection and associated complications are a leading cause of morbidity and mortality. It is appreciated that SIV is often complicated by secondary bacterial infection. Tracheal epithelial cells (TEC) and pulmonary cells respond to infection with proinflammatory cytokines for controlling pathogen spread; however, exacerbated responses can lead to immunopathology that may be detrimental to the host. The extent to which prior SIV infection alters host responses to secondary stimulation is poorly understood. Haemophilus parasuis is an important and common respiratory pathogen of pigs. The innate immune responses of the respiratory tract of pigs infected with SIV 5 days prior to secondary infection with H. parasuis were examined. The H. parasuis colonization was higher in the nose and lungs of SIV/Hps pigs compared to Hps-only pigs. These results indicate that influenza virus infection contributes enhanced bacterial colonization. In SIV/Hps pigs, IL-8, IL-6 and IL-1beta protein levels were increased in the tracheal wash and BAL, and TEC and BAL cells IL-8, IL-6 and IL-1beta mRNA expression levels were significantly increased over SIV-only and Hps-only pigs. This data provides support to the hypothesis that prior influenza infection alters subsequent immune responses.