4.7 Article

TREM1: A positive regulator for inflammatory response via NF-κB pathway in A549 cells infected with Mycoplasma pneumoniae

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 107, Issue -, Pages 1466-1472

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.07.176

Keywords

Mycoplasma pneumonia; A549 cells; TREM1; NF-kappa B

Funding

  1. Important Weak Subject Construction Project of Pudong Health and Family Planning Commission of Shanghai [PWZbr2017-23]

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Herein, we found that serum content of the triggering receptor expressed on myeloid cells-1 (TREM1) was increased, and positively correlated with Mycoplasma pneumoniae (MP)-DNA in children with MP infection. In this study, A549 cells, known as human lung epithelial cells, were co-cultured with 10(7) CCU/ml of MP to established in vitro model of MP infection. We studied the roles of TREM1 in inflammatory response of A549 cell by regulating the secretions of cytokine interleukin (IL)-8 and tumor necrosis factor (TNF)-alpha in cell culture supernatants. Moreover, transcriptional activity of nuclear factor kappa B (NF-kappa B) was assessed by measuring protein levels of NF-kappa B in the cytoplasm and nuclear. Our data suggested that sanguinarine chloride significantly decreased TREM1 expression, and alleviated inflammatory response of MP-infected A549 cells via preventing NF-kappa B nuclear translocation. To study the roles of TREM1 in inflammatory regulation in MP-infected A549 cells and the underlying mechanisms, we established TREM1 overexpression transfected A549 cells. PDTC was used for inhibiting NF-kappa B nuclear translocation. We found that TREM1 overexpression induced server inflammatory response of A549 cells. Besides, TREM1 overexpression attenuated anti-inflammatory effects of sanguinarine chloride in MP-infected cells. More importantly, pro-inflammatory effects of TREM1 overexpression was significantly reversed with additional PDTC treatment in MP-infected cells treated with sanguinarine chloride, suggesting that TREM1 was a pro-inflammatory factor via regulating NF-kappa B nuclear translocation in MP-infected A549 cells.

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