Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila
Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.5-induced lung injury. Additionally, gut microbiota and inflam...
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324017019 |
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| author | Li Wang Zhipeng Li Huan He Lijing Qin Weiqiang Xu Hongyuan Tian Rongrong Liu Xinru Lian Wen Li Yali Qi Zhicheng Wang |
| author_facet | Li Wang Zhipeng Li Huan He Lijing Qin Weiqiang Xu Hongyuan Tian Rongrong Liu Xinru Lian Wen Li Yali Qi Zhicheng Wang |
| author_sort | Li Wang |
| collection | DOAJ |
| description | Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.5-induced lung injury. Additionally, gut microbiota and inflammation are crucial in lung injury and the health benefits of LDR through gut microbiota need further exploration. Here, we aim to investigate the impact of LDR on PM2.5-induced lung injury in vivo and in vitro, and elucidated the potential mechanisms of anti-inflammation activated by gut microbiota. We observed that LDR ameliorated the lung damage induced by PM2.5 in mice. Additionally, after PM2.5 exposure, M1 polarization of macrophages in alveolar lavage fluid and Th1 polarization in spleen increased, pro-inflammatory cytokines (IL-1, IL-6 and TNF-α) increased and anti-inflammatory cytokines (IL-4, IL-10 and TGF-β) decreased in lung and serum. LDR could deteriorate the changes described as above. Intriguingly, Akkermansia muciniphila (Akk) differed most significantly in the gut microbiota of mice. Notably, PM2.5 activated the Toll-like receptors-induced MyD88/NF-κB pathways to mediate the pro-inflammation, and LDR could inhibited the pathway. However, the TLR1 and TLR2 continuously increased after LDR, indicating the downstream non-canonical TLR1/TLR2 pathway of Akk was activated to blunt the pro-inflammation of PM2.5. Our results strongly indicate that LDR-induced activation of gut Akk-dependent non-canonical TLR1/TLR2-like receptor pathway ameliorates lung injury and inflammation resulted from PM2.5. |
| format | Article |
| id | doaj-art-abdb6e45b54f422e8f2428ac55248091 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-abdb6e45b54f422e8f2428ac552480912025-01-23T05:25:54ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01289117625Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphilaLi Wang0Zhipeng Li1Huan He2Lijing Qin3Weiqiang Xu4Hongyuan Tian5Rongrong Liu6Xinru Lian7Wen Li8Yali Qi9Zhicheng Wang10NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaDepartment of Radiation Oncology, The First Medical Center of Chinese PLA General Hospital, Beijing 100853, China; Medical School of Chinese PLA, Beijing, ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR ChinaDepartment of Epidemiology, School of Public Health, Jilin Medical College, Jilin, Jilin 132013, PR ChinaNHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China; Corresponding author.Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.5-induced lung injury. Additionally, gut microbiota and inflammation are crucial in lung injury and the health benefits of LDR through gut microbiota need further exploration. Here, we aim to investigate the impact of LDR on PM2.5-induced lung injury in vivo and in vitro, and elucidated the potential mechanisms of anti-inflammation activated by gut microbiota. We observed that LDR ameliorated the lung damage induced by PM2.5 in mice. Additionally, after PM2.5 exposure, M1 polarization of macrophages in alveolar lavage fluid and Th1 polarization in spleen increased, pro-inflammatory cytokines (IL-1, IL-6 and TNF-α) increased and anti-inflammatory cytokines (IL-4, IL-10 and TGF-β) decreased in lung and serum. LDR could deteriorate the changes described as above. Intriguingly, Akkermansia muciniphila (Akk) differed most significantly in the gut microbiota of mice. Notably, PM2.5 activated the Toll-like receptors-induced MyD88/NF-κB pathways to mediate the pro-inflammation, and LDR could inhibited the pathway. However, the TLR1 and TLR2 continuously increased after LDR, indicating the downstream non-canonical TLR1/TLR2 pathway of Akk was activated to blunt the pro-inflammation of PM2.5. Our results strongly indicate that LDR-induced activation of gut Akk-dependent non-canonical TLR1/TLR2-like receptor pathway ameliorates lung injury and inflammation resulted from PM2.5.http://www.sciencedirect.com/science/article/pii/S0147651324017019PM2.5Lung injuryLow-dose radiationAkkermansia muciniphilaNon-canonical TLR1/TLR2-like receptor pathway |
| spellingShingle | Li Wang Zhipeng Li Huan He Lijing Qin Weiqiang Xu Hongyuan Tian Rongrong Liu Xinru Lian Wen Li Yali Qi Zhicheng Wang Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila Ecotoxicology and Environmental Safety PM2.5 Lung injury Low-dose radiation Akkermansia muciniphila Non-canonical TLR1/TLR2-like receptor pathway |
| title | Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila |
| title_full | Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila |
| title_fullStr | Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila |
| title_full_unstemmed | Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila |
| title_short | Low-dose radiation ameliorates PM2.5-induced lung injury through non-canonical TLR1/TLR2-like receptor pathways modulated by Akkermansia muciniphila |
| title_sort | low dose radiation ameliorates pm2 5 induced lung injury through non canonical tlr1 tlr2 like receptor pathways modulated by akkermansia muciniphila |
| topic | PM2.5 Lung injury Low-dose radiation Akkermansia muciniphila Non-canonical TLR1/TLR2-like receptor pathway |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324017019 |
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