Glaesserella parasuis infection triggers endoplasmic reticulum stress-mediated pyroptosis via PERK/eIF2α/ATF4 axis and metabolic reprogramming in porcine alveolar macrophages.

ABSTRACT: Glaesserella parasuis, the causative agent of Glässer's disease in swine, triggers severe systemic inflammation; however, the molecular mechanisms underpinning its pathogenesis remain incompletely understood. This study investigated the cellular and metabolic responses of porcine alveolar macrophage 3D4/21 cells to G. parasuis infection. Exposure to the pathogen significantly reduced cell viability and up-regulated pro-inflammatory cytokines (IL-6, IL-8, IL-1β, and TNF-α). Mechanistically, G. parasuis-induced apoptosis via up-regulation of Bcl-2-associated X protein (Bax) and cleaved Caspase-3, coupled with down-regulation of B-cell lymphoma-2 (Bcl-2). By contrast, pyroptosis was characterised by activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, Cas

SUBMITTER: Feng W 

PROVIDER: S-EPMC12265192 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature