Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae
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J Biosci (2020)45:133 DOI: 10.1007/s12038-020-00105-7
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Superoxide dismutase 3 as an inflammatory suppressor in A549 cells infected with Mycoplasma pneumoniae JIA-YUAN JIN1, , YE CHEN2, , XING-YOU WANG3, CHEN-MING LI1, WEI-LIN CHEN1 and LI LI1* 1
Department of Pharmacy, Puxing Community Health Service Center, 250 Gui Chang Road, Pudong New District, Shanghai 200129, People’s Republic of China
2
Department of Pharmacy, Sanlin Dekang Community Health Service Center, 375 San Lin Road, Pudong New District, Shanghai, People’s Republic of China 3
Management Institute of West China Hospital, Sichuan University, No. 2074, Water Tower, Wuhou District, Chengdu 610041, People’s Republic of China *Corresponding author (Email, [email protected])
These authors contributed equally to this work.
MS received 2 March 2019; accepted 1 October 2019 Herein, we found that serum concentration of superoxide dismutase 3 (SOD3) was significantly reduced in children with mycoplasma pneumonia (MP) infection. To study the roles of SOD3 in inflammatory regulation of MP infection, human A549 type II alveolar epithelial cells were stimulated with 107 CCU/ml of MP to build MP 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 response of A549 cells. Levofloxacin (LVFX) was used as an anti-inflammatory drug while recombinant TNF-a was used as an inflammatory promotor in MP-infected cells. Transcriptional activity of nuclear factor (NF)-rB was assessed by detecting protein levels of nuclear NF-rB and cytoplasm NF-rB using Western blot analysis. Our data suggested that the expression of SOD3 mRNA and protein, as well as content of SOD3 in cultured supernatant, were time-dependently inhibited in MP-infected A549 cells. However, lentiviruses-mediated SOD3 overexpression alleviated inflammatory response of MP-infected A549 cells, and prevented the unclear translocation of NF-rB, as evidenced by obviously reducing the production of IL-8 and TNF-a in cell cultured supernatant, as well as decreasing nuclear NF-rB while increasing cytoplasm NF-rB. Inspiringly, SOD3 overexpression induced anti-inflammatory effect and the inactivation of NF-rB was similar to that of 2 lg/ml of LVFX, but reversed by additional TNF-a treatment. Therefore, we can conclude that transcriptional activity of NF-jB was the underlying mechanism, by which SOD3 regulated inflammatory response in MP infection in vitro. Keywords.
A549 cells; mycoplasma pneumonia; NF-rB
1. Introduction Mycoplasma pneumoniae (MP), a gram-negative microorganism, has lipoproteins or lipopeptides with powerful inflammatory property (Saraya 2017), and is widely considered as the most common cause for community-acquired pneumonia among children over five years (Atkinson and Waites 2014; Kumar 2018). http://www.ias.ac.in/jbiosci
Commonly, after MP infection, there is an incubation period of 2–3 weeks in human body, followed by
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