Actinobacillus Pleuropneumoniae Pathogenesis and Immune Response

Actinobacillus pleuropneumoniae is a Gram-negative bacterium responsible for porcine pleuropneumonia, a severe respiratory disease characterised by fibrinous inflammation of the lungs and pleura. Pathogenesis begins with colonisation of the upper respiratory tract and adhesion to tracheal epithelium via specialised adhesins, leading to necrotic lung lesions mediated by a family of RTX toxins. The bacterium evades innate immunity through inhibition of respiratory burst in alveolar macrophages, interference with cytokine production and biofilm formation. Host defence relies on mucosal immunity, recruitment of neutrophils and macrophages, and activation of pattern-recognition receptors such as Toll-like receptor 4, which recognises bacterial lipopolysaccharide and triggers downstream signalling cascades. Adaptive immunity involves both humoral responses, notably antibody production against capsular polysaccharides and exotoxins, and cell-mediated responses that clear intracellular bacteria. Disease control and vaccine strategies have focused on subunit vaccines targeting surface antigens, toxin derivatives and conserved outer membrane proteins to elicit robust protection while minimising pathological inflammation. Advances in genomics and proteomics have deepened understanding of virulence mechanisms and prompted exploration of novel therapeutic approaches to mitigate economic losses in swine production globally.

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Actinobacillus Pleuropneumoniae Pathogenesis and Immune Response publication trend

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Technical terms

Pleuropneumonia: Inflammation of the lung parenchyma and pleural membranes leading to fibrinous exudate and tissue necrosis.

Alveolar macrophage: Phagocytic immune cell resident in the lung alveoli that engulfs and destroys pathogens.

Autotransporter adhesion (Adh): A self-secreted bacterial surface protein that mediates attachment to host cells and contributes to immune evasion.

Reactive oxygen species (ROS): Highly reactive molecules produced by immune cells that destroy pathogens during the respiratory burst.

Tight junction: Complexes of transmembrane proteins that seal epithelial cells together, maintaining barrier integrity.

Toll-like receptor 4 (TLR4): Innate immune receptor that recognises bacterial lipopolysaccharide and initiates pro-inflammatory signalling.

Mitogen-activated protein kinase (MAPK): Enzyme family that transduces extracellular signals to regulate cellular responses such as inflammation.

Protein kinase C (PKC): Enzyme involved in signal transduction pathways controlling cell proliferation and barrier function.

Myosin light chain kinase (MLCK): Enzyme that phosphorylates myosin light chains to modulate cytoskeletal dynamics and junctional permeability.

References

1. De novo identification of bacterial antigens of a clinical isolate by combining use of proteosurfaceomics, secretomics, and BacScan technologies. Frontiers in Immunology (2023).
2. Adh Promotes Actinobacillus pleuropneumoniae Survival in Porcine Alveolar Macrophages by Inhibiting CHAC2-Mediated Respiratory Burst and Inflammatory Cytokine Expression. Cells (2023).
3. Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling. International Journal of Molecular Sciences (2023).