# Simulated poultry-house PM2.5 exposure reveals a gut–lung axis mechanism of microbial propionate in protecting against pneumonia

## TL;DR

Exposure to poultry house PM2.5 harms lungs and gut health, but adding beneficial bacteria or propionate can reduce inflammation and protect poultry.

## Contribution

This study identifies a gut–lung axis mechanism linking PM2.5 exposure to pneumonia and shows how microbial propionate can counteract it.

## Key findings

- PM2.5 exposure disrupts lung structure and increases inflammatory markers like IL-1β and IL-6.
- Gut microbiota shifts toward pro-inflammatory taxa and away from SCFA producers like Bacteroides uniformis.
- Supplementing with B. uniformis or propionate reduces lung inflammation and restores immune balance.

## Abstract

Poultry house fine particulate matter (PM2.5) 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 PM2.5 (2 mg/m³, 2 h/day) to investigate pulmonary injury and gut–lung axis perturbations. PM2.5 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 PM2.5-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.

This study reveals that poultry house-derived PM2.5 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 PM2.5 exposure and supports sustainable, non-antibiotic interventions to enhance animal welfare and productivity under deteriorating air quality conditions.