Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae
dc.contributor.author | Jin, Jia-Yuan | en_US |
dc.contributor.author | Chen, Ye | en_US |
dc.contributor.author | Wang, Xing-You | en_US |
dc.contributor.author | Li, Chen-Ming | en_US |
dc.contributor.author | Chen, Wei-Lin | en_US |
dc.contributor.author | Li, Li | en_US |
dc.date.accessioned | 2020-11-18T10:14:14Z | |
dc.date.available | 2020-11-18T10:14:14Z | |
dc.date.issued | 2020-10 | |
dc.description.abstract | Herein, we found that serum concentration of superoxide dismutase 3 (SOD3) was significantly reduced inchildren with mycoplasma pneumonia (MP) infection. To study the roles of SOD3 in inflammatory regulationof MP infection, human A549 type II alveolar epithelial cells were stimulated with 107 CCU/ml of MP to buildMP infection in vitro. Secretion of pro-inflammatory cytokine interleukin (IL)-8 and tumor necrosis factor(TNF)-a were measured via enzyme-linked immunosorbent assay (ELISA) to assess the inflammatory responseof A549 cells. Levofloxacin (LVFX) was used as an anti-inflammatory drug while recombinant TNF-a wasused as an inflammatory promotor in MP-infected cells. Transcriptional activity of nuclear factor (NF)-rB wasassessed by detecting protein levels of nuclear NF-rB and cytoplasm NF-rB using Western blot analysis. Ourdata suggested that the expression of SOD3 mRNA and protein, as well as content of SOD3 in culturedsupernatant, were time-dependently inhibited in MP-infected A549 cells. However, lentiviruses-mediatedSOD3 overexpression alleviated inflammatory response of MP-infected A549 cells, and prevented the uncleartranslocation of NF-rB, as evidenced by obviously reducing the production of IL-8 and TNF-a in cell culturedsupernatant, as well as decreasing nuclear NF-rB while increasing cytoplasm NF-rB. Inspiringly, SOD3overexpression induced anti-inflammatory effect and the inactivation of NF-rB was similar to that of 2 lg/mlof LVFX, but reversed by additional TNF-a treatment. Therefore, we can conclude that transcriptional activityof NF-jB was the underlying mechanism, by which SOD3 regulated inflammatory response in MP infectionin vitro | en_US |
dc.identifier.affiliations | Department of Pharmacy, Puxing Community Health Service Center, 250 Gui Chang Road, Pudong New District, Shanghai 200129, People’s Republic of China | en_US |
dc.identifier.affiliations | Department of Pharmacy, Sanlin Dekang Community Health Service Center, 375 San Lin Road, Pudong New District, Shanghai, People’s Republic of China | en_US |
dc.identifier.affiliations | Management Institute of West China Hospital, Sichuan University, No. 2074, Water Tower, Wuhou District, Chengdu 610041, People’s Republic of China | en_US |
dc.identifier.affiliations | Department of Pharmacy, Puxing Community Health Service Center, 250 Gui Chang Road, Pudong New District, Shanghai 200129, People’s Republic of China | en_US |
dc.identifier.citation | Jin Jia-Yuan, Chen Ye, Wang Xing-You, Li Chen-Ming, Chen Wei-Lin, Li Li. Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae. Journal of Biosciences. 2020 Oct; : 1-7 | en_US |
dc.identifier.issn | 0250-5991 | |
dc.identifier.issn | 0973-7138 | |
dc.identifier.place | India | en_US |
dc.identifier.uri | https://imsear.searo.who.int/handle/123456789/214221 | |
dc.language | en | en_US |
dc.publisher | Indian Academy of Sciences | en_US |
dc.relation.volume | 45 | en_US |
dc.source.uri | https://dx.doi.org//10.1007/s12038-020-00105-7 | en_US |
dc.subject | A549 cells | en_US |
dc.subject | mycoplasma pneumonia | en_US |
dc.subject | NF-rB | en_US |
dc.title | Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae | en_US |
dc.type | Journal Article | en_US |
Files
Original bundle
1 - 1 of 1