PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway
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 ar...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-06-01
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| Series: | Frontiers in Pharmacology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2022.924242/full |
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| author | Jianlong Zhang Jianlong Zhang Jianlong Zhang Chong Liu Chong Liu Guangrong Zhao Guangrong Zhao Guangrong Zhao Meng Li Di Ma Di Ma Qingguo Meng Wenli Tang Qingrong Huang Qingrong Huang Peimin Shi Youzhi Li Linlin Jiang Linlin Jiang Linlin Jiang Xin Yu Xin Yu Xin Yu Hongwei Zhu Hongwei Zhu Hongwei Zhu Guozhong Chen Guozhong Chen Guozhong Chen Xingxiao Zhang Xingxiao Zhang Xingxiao Zhang |
| author_facet | Jianlong Zhang Jianlong Zhang Jianlong Zhang Chong Liu Chong Liu Guangrong Zhao Guangrong Zhao Guangrong Zhao Meng Li Di Ma Di Ma Qingguo Meng Wenli Tang Qingrong Huang Qingrong Huang Peimin Shi Youzhi Li Linlin Jiang Linlin Jiang Linlin Jiang Xin Yu Xin Yu Xin Yu Hongwei Zhu Hongwei Zhu Hongwei Zhu Guozhong Chen Guozhong Chen Guozhong Chen Xingxiao Zhang Xingxiao Zhang Xingxiao Zhang |
| author_sort | Jianlong Zhang |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-13T19:10:28Z |
| format | Article |
| id | doaj.art-9669573132f94069ba65ecbcfdcc5785 |
| institution | Directory Open Access Journal |
| issn | 1663-9812 |
| language | English |
| last_indexed | 2024-04-13T19:10:28Z |
| publishDate | 2022-06-01 |
| publisher | Frontiers Media S.A. |
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| series | Frontiers in Pharmacology |
| spelling | doaj.art-9669573132f94069ba65ecbcfdcc57852022-12-22T02:33:52ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122022-06-011310.3389/fphar.2022.924242924242PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR PathwayJianlong Zhang0Jianlong Zhang1Jianlong Zhang2Chong Liu3Chong Liu4Guangrong Zhao5Guangrong Zhao6Guangrong Zhao7Meng Li8Di Ma9Di Ma10Qingguo Meng11Wenli Tang12Qingrong Huang13Qingrong Huang14Peimin Shi15Youzhi Li16Linlin Jiang17Linlin Jiang18Linlin Jiang19Xin Yu20Xin Yu21Xin Yu22Hongwei Zhu23Hongwei Zhu24Hongwei Zhu25Guozhong Chen26Guozhong Chen27Guozhong Chen28Xingxiao Zhang29Xingxiao Zhang30Xingxiao Zhang31School of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaSchool of Pharmacy, Yantai University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaYantai Key Laboratory of Animal Pathogenetic Microbiology and Immunology, Yantai, ChinaLinyi Central Blood Station, Linyi, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaYantai Key Laboratory of Animal Pathogenetic Microbiology and Immunology, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji’nan, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaYantai Key Laboratory of Animal Pathogenetic Microbiology and Immunology, Yantai, ChinaSchool of Life Sciences, Ludong University, Yantai, ChinaShandong Breeding Environmental Control Engineering Laboratory, Yantai, ChinaYantai Key Laboratory of Animal Pathogenetic Microbiology and Immunology, Yantai, ChinaHigh 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.https://www.frontiersin.org/articles/10.3389/fphar.2022.924242/fullPM2.5Pseudomonas aeruginosaalveolar macrophagespoultry housesmTOR |
| spellingShingle | Jianlong Zhang Jianlong Zhang Jianlong Zhang Chong Liu Chong Liu Guangrong Zhao Guangrong Zhao Guangrong Zhao Meng Li Di Ma Di Ma Qingguo Meng Wenli Tang Qingrong Huang Qingrong Huang Peimin Shi Youzhi Li Linlin Jiang Linlin Jiang Linlin Jiang Xin Yu Xin Yu Xin Yu Hongwei Zhu Hongwei Zhu Hongwei Zhu Guozhong Chen Guozhong Chen Guozhong Chen Xingxiao Zhang Xingxiao Zhang Xingxiao Zhang PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway Frontiers in Pharmacology PM2.5 Pseudomonas aeruginosa alveolar macrophages poultry houses mTOR |
| title | PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway |
| title_full | PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway |
| title_fullStr | PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway |
| title_full_unstemmed | PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway |
| title_short | PM2.5 Synergizes With Pseudomonas aeruginosa to Suppress Alveolar Macrophage Function in Mice Through the mTOR Pathway |
| title_sort | pm2 5 synergizes with pseudomonas aeruginosa to suppress alveolar macrophage function in mice through the mtor pathway |
| topic | PM2.5 Pseudomonas aeruginosa alveolar macrophages poultry houses mTOR |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2022.924242/full |
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