Simulated poultry-house PM(2.5) exposure reveals a gut-lung axis mechanism of microbial propionate in protecting against pneumonia.

Poultry house fine particulate matter (PM(2.5)) poses significant respiratory risks to poultry by penetrating deep into the lung and triggering inflammatory cascades. In this study, 21- to 28-day-old broilers were exposed to total suspended particulates enriched in PM(2.5) (2 mg/m³, 2 h/day) to investigate pulmonary injury and gut-lung axis perturbations. PM(2.5) exposure induced collapse of the hexagonal lobular architecture, elevated pulmonary expression of IL-1β, IL-2, IL-6, IL-8, and IL-10, and activated NF-κB signaling. Concurrently, cecal microbiota α-diversity increased while the community shifted toward pro-inflammatory taxa (Alistipes, Rikenellaceae) and away from SCFA-producing species (Bacteroides uniformis, Parabacteroides). Oral supplementation of B. uniformis restored its abundance, replenished acetate and propionate levels, and attenuated lung injury by reducing APC activation (CD40, CCL4) and Th1 polarization (T-bet, IFN-γ, IL-18), while promoting regulatory T cell markers (FoxP3). Dietary sodium propionate supplementation in feed (0.4%) similarly mitigated pulmonary inflammation and Th1 skewing, albeit without enhancing Treg responses. These findings demonstrate that PM(2.5)-induced lung damage is intricately linked to gut dysbiosis and SCFA depletion and that restoration of B. uniformis or its metabolite propionate can recalibrate the gut-lung axis to suppress innate and adaptive inflammatory pathways. This work highlights microbiota- and metabolite-based interventions as promising strategies to protect poultry respiratory health and performance under air-polluted conditions.IMPORTANCEThis study reveals that poultry house-derived PM(2.5) not only causes direct lung inflammation but also perturbs the gut-lung axis by depleting beneficial SCFA-producing bacteria. The resulting gut dysbiosis amplifies respiratory immune injury, highlighting a previously underappreciated systemic effect of airborne pollutants in livestock environments. Our findings suggest that microbiota- and metabolite-targeted dietary strategies can mitigate air pollution-induced health risks in poultry. This work provides new insights into the broader ecological and agricultural consequences of PM(2.5) exposure and supports sustainable, non-antibiotic interventions to enhance animal welfare and productivity under deteriorating air quality conditions.