ArticleBMC veterinary research2017
Host-pathogen interplay at primary infection sites in pigs challenged with Actinobacillus pleuropneumoniae.
Article in BMC veterinary research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Immunization of pigs with Actinobacillus pleuropneumonia live attenuated (gene-deleted) vaccine HB04M intramuscularly or intranasally exhibits remarkably rapid protection against heterologous strain challenge.BMC veterinary research · 2025Article
- Examination of the Virulence ofVeterinary sciences · 2024Article
- Causes of Sow Mortality and Risks to Post-Mortem Findings in a Brazilian Intensive Swine Production System.Animals : an open access journal from MDPI · 2022Article
- Isolation of Biotype 1 Serotype 12 and Detection ofPathogens (Basel, Switzerland) · 2022Article
- The Connection Between Stress and Immune Status in Pigs: A First Salivary Analytical Panel for Disease Differentiation.Frontiers in veterinary science · 2022Article
- IFN-γInfection and immunity · 2021Article
- From Stable to Lab-Investigating Key Factors for Sudden Deaths Caused byPathogens (Basel, Switzerland) · 2019Article
- Degraded neutrophil extracellular traps promote the growth of Actinobacillus pleuropneumoniae.Cell death & disease · 2019Article
- Article
- Haptoglobin and C-Reactive Protein-Non-specific Markers for Nursery Conditions in Swine.Frontiers in veterinary science · 2019Article
- Activation of Porcine Alveolar Macrophages by Actinobacillus pleuropneumoniae Lipopolysaccharide via the Toll-Like Receptor 4/NF-κB-Mediated Pathway.Infection and immunity · 2018Article
- Anti-Inflammatory Benefits of Antibiotics: Tylvalosin Induces Apoptosis of Porcine Neutrophils and Macrophages, Promotes Efferocytosis, and Inhibits Pro-Inflammatory CXCL-8, IL1α, and LTBFrontiers in veterinary science · 2018Article
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActinobacillus (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.
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