ARS | Publication request: Antecedent Influenza Virus Infection Enhances Pulmonary Responses to Secondary Haemophilus Infection in a Porcine Co-Infection Model

Submitted to: American Association of Immunologists Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: January 24, 2010
Publication Date: June 1, 2010
Citation: Loving, C.L., Brockmeier, S.L., Vincent, A.L. 2010. Antecedent Influenza virus infection enhances pulmonary responses to secondary Haemophilus infection in a porcine co-infection model [abstract]. American Association of Immunologists. Paper No. 803219.

Technical Abstract: Influenza (Flu) infection and associated complications are a leading cause of morbidity and mortality worldwide. It is appreciated that Flu is complicated by secondary bacterial infection. Tracheal epithelial cells (TEC) and pulmonary macrophages (Mac) 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 antecedent Flu alters TEC and Mac responses to secondary stimulation is poorly understood. Pigs serve as a model for Flu infection, and secondary infection with Haemophilus parasuis (Hps) provides a useful co-infection model for evaluating host responses. Groups of pigs were infected with Flu virus and 5-days later infected with Hps (Flu/Hps). Non-infected, Flu-only and Hps-only groups were included as controls. Pigs were necropsied 1 day following Hps inoculation and results show Hps colonization was higher in the nose and lungs of Flu/Hps pigs compared to Hps-only pigs. In Flu/Hps pigs, IL-8, IL-6 and IL-1b protein levels were increased in the lung, and TEC and Mac IL-8, IL-6 and IL-1b mRNA expression levels were significantly increased over Flu-only and Hps-only pigs. In addition, TEC and Mac from 5-day post-Flu pigs exhibited dysregulated innate immune responses to secondary Hps exposure in vitro, providing additional evidence that Flu infection alters host responses to secondary stimulation.