Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: October 15, 2010
Publication Date: December 5, 2010
Citation: Loving, C.L., Brockmeier, S.L., Vincent, A.L. 2010. Innate immune responses are enhanced in pigs after sequential infection with influenza virus and Haemophilus parasuis [abstract]. Conference of Research Workers in Animal Diseases. Paper No. 165. Technical Abstract: Swine influenza virus (SIV) infection alone causes significant disease characterized by respiratory distress and poor growth. However, SIV also plays a significant role in the porcine respiratory disease complex (PRDC), though the mechanism in which this occurs is not clearly defined. Haemophilus parasuis (Hps) has been shown to be a complicating factor of influenza in pigs, and both agents continue to be isolated from pigs with pneumonia. After infection, the host immune response is critical for controlling pathogen spread and initiating the adaptive immune response. Tracheal epithelial cells (TEC) and pulmonary macrophages (Mac) are first responders during pulmonary infection with the production of proinflammatory cytokines. Influenza infection is known to predispose to secondary bacterial infection; however, the extent to which antecedent SIV alters TEC and Mac responses to secondary stimulation is poorly understood. To better understand the interaction between SIV and Hps in pigs, groups of pigs were infected with SIV and 5-days later infected with Hps (Flu/Hps). Non-infected, Flu-only and Hps-only groups served as controls. Pigs were necropsied 1 day following Hps inoculation and results show Hps colonization was higher in the nose and lungs of SIV/Hps pigs compared to Hps-only pigs. In SIV/Hps pigs, IL-8, IL-6 and IL-1beta protein levels were increased in the lung, and TEC and Mac cytokine mRNA expression levels were significantly increased over SIV-only and Hps-only pigs. Also, TEC and Mac from 5-day post-SIV pigs exhibited dysregulated innate immune responses to secondary Hps exposure in vitro, providing additional evidence that SIV infection alters host responses to secondary stimulation.