Gram-negative bacterial outer membrane proteins and lipopolysaccharides key factors linking chicken coop environment and oxidative stress.

High concentrations of particulate matter (PM) in poultry housing act as carriers for microbial aerosols, with Gram-negative bacteria and their outer membrane components-outer membrane proteins (OMPs) and lipopolysaccharide (LPS)-playing pivotal roles in disrupting redox homeostasis. This review systematically examines how OMPs and LPS drive mitochondrial dysfunction and oxidative damage, proposing the "mitochondrial-ROS axis" as an integrative framework to explain their convergent mechanisms. We evaluate evidence that OMPs promote iron dysregulation, target mitochondria, and initiate apoptotic signaling, whereas LPS triggers robust mitochondrial ROS bursts via TLR4/MyD88 and TRAF6-ECSIT pathways, leading to NLRP3 inflammasome activation and pyroptosis. And we further clarify the dynamic conflict between pathogen attack, mediated through the oxidative bursts of OMPs and LPS, and host reductive defenses, including peroxisomal activity, thioredoxin and glutathione systems, and uncoupling proteins. While this axis provides a useful predictive model for anticipating oxidative stress intensity and inflammatory activation, its applicability has notable constraints-such as the context-dependence of ROS in cell-fate decisions and the need for further avian-specific validation of key pathways. This synthesis provides a balanced perspective. Future studies should prioritize avian-specific validation of key pathways and elucidate the temporal dynamics and tissue specificity of ROS responses to inform targeted interventions in poultry health.