Abstract
Background Actinobacillus (A.) pleuropneumoniae is the causative agent of porcine pleuropneumonia and causes significant losses in the pig industry worldwide. Early host immune response is crucial for further progression of the disease. A. pleuropneumoniae is either rapidly eliminated by the immune system or switches to a long-term persistent form. To gain insight into the host-pathogen interaction during the early stages of infection, pigs were inoculated intratracheally with A. pleuropneumoniae serotype 2 and humanely euthanized eight hours after infection. Gene expression studies of inflammatory cytokines and the acute phase proteins haptoglobin, serum amyloid A and C-reactive protein were carried out by RT-qPCR from the lung, liver, tonsils and salivary gland. In addition, the concentration of cytokines and acute phase proteins were measured by quantitative immunoassays in bronchoalveolar lavage fluid, serum and saliva. In parallel to the analyses of host response, the impact of the host on the bacterial pathogen was assessed on a metabolic level. For the latter, Fourier-Transform Infrared (FTIR-) spectroscopy was employed.ResultsSignificant cytokine and acute phase protein gene expression was detected in the lung and the salivary gland however this was not observed in the tonsils. In parallel to the analyses of host response, the impact of the host on the bacterial pathogen was assessed on a metabolic level. For the latter investigations, Fourier-Transform Infrared (FTIR-) spectroscopy was employed. The bacteria isolated from the upper and lower respiratory tract showed distinct IR spectral patterns reflecting the organ-specific acute phase response of the host.ConclusionsIn summary, this study implies a metabolic adaptation of A. pleuropneumoniae to the porcine upper respiratory tract already during early infection, which might indicate a first step towards the persistence of A. pleuropneumoniae. Not only in lung, but also in the salivary gland an increased inflammatory gene expression was detectable during the acute stage of infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-017-0979-6) contains supplementary material, which is available to authorized users.
Highlights
Actinobacillus (A.) pleuropneumoniae is the causative agent of porcine pleuropneumonia and causes significant losses in the pig industry worldwide
We investigated the mRNA expression of inflammatory cytokines and acute phase proteins in the lung, liver, salivary gland and tonsils as well as the protein levels of these markers in bronchoalveolar lavage fluid (BALF), serum and saliva samples
Microscopic lung tissue alterations in infected pigs were dominated by a severe neutrophilic infiltration as well as fibrin exudation into the alveolar spaces and interalveolar septa leading to an obstruction of bronchioli (Fig. 1b)
Summary
Actinobacillus (A.) pleuropneumoniae is the causative agent of porcine pleuropneumonia and causes significant losses in the pig industry worldwide. Innate immune response to respiratory disease is not restricted to the lung as the primary site of infection, but involves peripheral lymphoid tissues, the liver [5] and the salivary gland [6]. For A. pleuropneumoniae the synergic action of endotoxins and the pore forming exotoxins Apx I to IV, in enhancing the production of inflammatory cytokines, such as IL-6, TNF-α and IL-1 is well known [5, 7,8,9]. These bacterial virulence factors can cause tissue damage, directly by Apx cytotoxic effect and indirectly by mounting an exacerbated inflammatory response
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