Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae

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dc.contributor.authorJin, Jia-Yuanen_US
dc.contributor.authorChen, Yeen_US
dc.contributor.authorWang, Xing-Youen_US
dc.contributor.authorLi, Chen-Mingen_US
dc.contributor.authorChen, Wei-Linen_US
dc.contributor.authorLi, Lien_US
dc.date.accessioned2020-11-18T10:14:14Z
dc.date.available2020-11-18T10:14:14Z
dc.date.issued2020-10
dc.description.abstractHerein, 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 vitroen_US
dc.identifier.affiliationsDepartment of Pharmacy, Puxing Community Health Service Center, 250 Gui Chang Road, Pudong New District, Shanghai 200129, People’s Republic of Chinaen_US
dc.identifier.affiliationsDepartment of Pharmacy, Sanlin Dekang Community Health Service Center, 375 San Lin Road, Pudong New District, Shanghai, People’s Republic of Chinaen_US
dc.identifier.affiliationsManagement Institute of West China Hospital, Sichuan University, No. 2074, Water Tower, Wuhou District, Chengdu 610041, People’s Republic of Chinaen_US
dc.identifier.affiliationsDepartment of Pharmacy, Puxing Community Health Service Center, 250 Gui Chang Road, Pudong New District, Shanghai 200129, People’s Republic of Chinaen_US
dc.identifier.citationJin 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; : 1-7en_US
dc.identifier.issn0250-5991
dc.identifier.issn0973-7138
dc.identifier.placeIndiaen_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/214221
dc.languageenen_US
dc.publisherIndian Academy of Sciencesen_US
dc.relation.volume45en_US
dc.source.urihttps://dx.doi.org//10.1007/s12038-020-00105-7en_US
dc.subjectA549 cellsen_US
dc.subjectmycoplasma pneumoniaen_US
dc.subjectNF-rBen_US
dc.titleSuperoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniaeen_US
dc.typeJournal Articleen_US
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