Publication details

Immune response of porcine alveolar macrophages to a concurrent infection with porcine reproductive and respiratory syndrome virus and Haemophilus parasuis in vitro

Authors

KAVANOVÁ Lenka PRODĚLALOVÁ Jana NEDBALCOVÁ Kateřina MATIAŠOVIC Ján VOLF Jiří FALDYNA Martin SALÁT Jiří

Year of publication 2015
Type Article in Periodical
Magazine / Source Veterinary Microbiology
MU Faculty or unit

Faculty of Science

Citation
web http://www.sciencedirect.com/science/article/pii/S0378113515300158
Doi http://dx.doi.org/10.1016/j.vetmic.2015.08.026
Field Immunology
Keywords Haemophilus parasuis; IL-1beta; PRRSV; Porcine alveolar macrophages; Reactive oxygen species
Description Porcine reproductive and respiratory syndrome virus (PRRSV) can predispose pigs to secondary respiratory infection with bacteria such as Haemophilus parasuis. Animals infected with both pathogens develop more severe clinical disease. The immune response of porcine alveolar macrophages (PAMs) to simultaneous infection with PRRSV and H. parasuis was analysed in vitro, describing cytokine production, expression of cell surface molecules, and production of reactive oxygen species (ROS). Concurrent infection with PRRSV and H. parasuis increased gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1 beta, IL-8) in PAMs in comparison with PAMs infected with PRRSV or H. parasuis alone. An additive effect of dual infection on IL-1 beta production was confirmed at the protein level. PAMs infected with PRRSV showed increased production of ROS compared to controls. Conversely, simultaneous infection of PAMs with PRRSV and H. parasuis decreased production of ROS, indicating the presence of an H. parasuis defence mechanism against respiratory burst. Concurrent infection of PAMs with PRRSV and H. parasuis was shown to elicit a pro-inflammatory immune response represented by significant IL-1 beta production. Severe multifactorial respiratory disease in natural conditions caused by both pathogens could be the consequence of pro-inflammatory mediated immunopathology.

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