Abstract
BackgroundThe bacterium Actinobacillus pleuropneumoniae is responsible for porcine pleuropneumonia, a widespread, highly contagious and often fatal respiratory disease of pigs. The general porcine innate immune response after A. pleuropneumoniae infection is still not clarified. The objective of this study was hence to characterise the transcriptional response, measured by using cDNA microarrays, in pigs 24 hours after experimental inoculation with A. pleuropneumoniae.MethodsMicroarray analyses were conducted to reveal genes being differentially expressed in inflamed versus non-inflamed lung tissue sampled from inoculated animals as well as in liver and tracheobronchial lymph node tissue sampled from three inoculated animals versus two non-inoculated animals. The lung samples were studied using a porcine cDNA microarray with 5375 unique PCR products while liver tissue and tracheobronchial lymph node tissue were hybridised to an expanded version of the porcine microarray with 26879 unique PCR products.ResultsA total of 357 genes differed significantly in expression between infected and non-infected lung tissue, 713 genes differed in expression in liver tissue from infected versus non-infected animals and 130 genes differed in expression in tracheobronchial lymph node tissue from infected versus non-infected animals. Among these genes, several have previously been described to be part of a general host response to infections encoding immune response related proteins. In inflamed lung tissue, genes encoding immune activating proteins and other pro-inflammatory mediators of the innate immune response were found to be up-regulated. Genes encoding different acute phase reactants were found to be differentially expressed in the liver.ConclusionThe obtained results are largely in accordance with previous studies of the mammalian immune response. Furthermore, a number of differentially expressed genes have not previously been associated with infection or are presently unidentified. Determination of their specific roles during infection may lead to a better understanding of innate immunity in pigs. Although additional work including more animals is clearly needed to elucidate host response to porcine pleuropneumonia, the results presented in this study demonstrate three subsets of genes consistently expressed at different levels depending upon infection status.
Highlights
The bacterium Actinobacillus pleuropneumoniae is responsible for porcine pleuropneumonia, a widespread, highly contagious and often fatal respiratory disease of pigs
Infection of the porcine lung with A. pleuropneumoniae has previously been reported to result in a local production of proinflammatory proteins or mRNA encoding the cytokines interleukin (IL) -1α, IL-1β, IL-6 and the chemokine IL-8 [2,3,4,5]
Necropsy findings One pig died within 24 hours and by necropsy the lungs were severely affected by acute, multifocal, fibrinonecrotizing and hemorrhagic pneumonia complicated with acute diffuse fibrinous pleuritis
Summary
The bacterium Actinobacillus pleuropneumoniae is responsible for porcine pleuropneumonia, a widespread, highly contagious and often fatal respiratory disease of pigs. Likewise bioactive protein and/or mRNA coding for IL10, IL12p35, TNF- α and INF α have been shown to be upregulated after infection with A. pleuropneumoniae in vivo or in vitro [2,3,4,5,6,7,8]. These studies have focused on a few selected genes using techniques such as quantitative realtime reverse transcriptase polymerase chain reactions (RTPCR), northern blotting or in-situ hybridisation. Using cDNA microarrays Moser and co-workers found 307 anonymous transcripts in blood leukocytes from pigs to be significantly affected after experimental infection with A. pleuropneumoniae [9]
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