Host-pathogen interplay at primary infection sites in pigs challenged with Actinobacillus pleuropneumoniae

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.

Update onActinobacillus pleuropneumoniae-knowledge, gaps and challenges

“…Infection of the tonsils may occur without induction of an immune response, especially against toxins (Chiers, Donné, Van Overbeke, Ducatelle, & Haesebrouck, ), thus impairing the detection of subclinically infected animals (Gottschalk, ). Recently, a host–pathogen study reported low immunological responsiveness in tonsils and showed, in parallel, that App isolates from this host compartment undertake distinct metabolic adaptations to the upper respiratory tract as early as 8 hrs after App intratracheal infection (Sassu, Frombling, et al., ).…”

“…Recently, a host-pathogen study reported low immunological responsiveness in tonsils and showed, in parallel, that App isolates from this host compartment undertake distinct metabolic adaptations to the upper respiratory tract as early as 8 hrs after App intratracheal infection (Sassu, Frombling, et al, 2017).…”

From Stable to Lab—Investigating Key Factors for Sudden Deaths Caused by Streptococcus suis

“…One lung lobe was lavaged after separation from the carcass with 400 mL of sterile PBS to collect BALF as previously described [67]. The BALF was centrifuged (400× g at room temperature) and frozen in aliquots at −80 • C.…”

Activation of Porcine Alveolar Macrophages by Actinobacillus pleuropneumoniae Lipopolysaccharide via the Toll-Like Receptor 4/NF-κB-Mediated Pathway

“…Alveolar macrophages are resident phagocytes of the alveolar space (31). Recent studies with animals with acute lung injury have indicated that an uncontrolled inflammatory response in PAMs is important in the pathogenesis of pleural pneumonia (2,4,5). Moreover, much research on macrophages has focused on the secretion of cytokines (32)(33)(34)(35).…”

“…A. pleuropneumoniae can be divided into two biotypes (biotype 1 and biotype 2), with biotype 1 having 12 serotypes and biotype 2 having 6 serotypes (3). The virulence of each serotype varies according to the Apx toxins and the surface lipopolysaccharide (LPS) (4). LPS extracted from A. pleuropneumoniae serotype 1 was suggested to be involved in lung infection (5)(6)(7)(8).…”