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Updated: Sep 5, 2025

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR
Jianlong Zhang1,2,3, Chong Liu1,2, Guangrong Zhao1,2,3
1School of Life Sciences, Ludong University, Yantai, China.
Abstract:
High concentrations of PM2.5 in enclosed broiler houses cause respiratory disorders in humans and animals. Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen that can induce severe respiratory disease in animals under stress or with abnormal immune functions. Alveolar macrophages are lung-resident immune cells that play important roles in lung host defence and immune balance. In this study, the mechanism by which PM2.5 synergizes with P. aeruginosa to damage alveolar macrophage function and induce inflammation was investigated. The results will provide a theoretical basis for improving the poultry breeding environment and preventing the recurrence of infection with P. aeruginosa. Alveolar macrophages were stimulated by PM2.5 collected in an enclosed broiler house and P. aeruginosa. Phagocytosis was determined by the neutral red test. The apoptosis rate and cytoskeleton changes were observed by flow cytometry assays and laser scanning confocal microscopy. Protein levels related to autophagy and the mTOR pathway were detected by Western blotting. The results indicated that PM2.5 in combination with P. aeruginosa could decrease phagocytosis, inhibit autophagy, increase apoptosis, and destroy the cytoskeleton in alveolar macrophages. In addition, alveolar macrophages had significantly increased expression of mTOR pathway-related proteins in response to the synergistic stimulation of PM2.5 and P. aeruginosa. The above results confirmed that PM2.5 in poultry houses synergized with P. aeruginosa to impede alveolar macrophage function and caused more severe respiratory system injuries through a process closely related to the activation of the mTOR signalling pathway.
Insights
Fine particulate matter (PM2.5) and Pseudomonas aeruginosa synergize to impair broiler chicken lung immune cells. This interaction, linked to mTOR pathway activation, increases respiratory disease risk in poultry.
Area of Science:
- Environmental Toxicology
- Immunology
- Poultry Science
Background:
- High PM2.5 concentrations in broiler houses are linked to respiratory issues.
- Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen causing severe respiratory disease, especially in immunocompromised animals.
- Alveolar macrophages are crucial for lung defense and immune homeostasis.
Purpose of the Study:
- To investigate the synergistic mechanism of PM2.5 and P. aeruginosa on alveolar macrophage function.
- To elucidate the role of the mTOR pathway in PM2.5 and P. aeruginosa-induced inflammation.
- To provide a basis for improving poultry environments and preventing P. aeruginosa infections.
Main Methods:
- Alveolar macrophages were stimulated with PM2.5 and P. aeruginosa.
- Phagocytosis assessed via neutral red test.
- Apoptosis and cytoskeleton changes analyzed by flow cytometry and confocal microscopy.
- Autophagy and mTOR pathway proteins quantified using Western blotting.
Main Results:
- Combined PM2.5 and P. aeruginosa exposure reduced phagocytosis and inhibited autophagy.
- Increased apoptosis and cytoskeleton disruption were observed in alveolar macrophages.
- Synergistic stimulation significantly upregulated mTOR pathway-related proteins.
Conclusions:
- PM2.5 and P. aeruginosa synergistically impair alveolar macrophage function in poultry houses.
- This impairment leads to more severe respiratory injuries, closely involving mTOR pathway activation.
- Findings highlight the need for environmental improvements to mitigate synergistic effects.

