Pseudomonas aeruginosa quorum-sensing signaling molecule N-3-oxododecanoyl homoserine lactone induces matrix metalloproteinase 9 expression via the AP1 pathway in rat fibroblasts. Issue 10 (3rd October 2015)

• Record Type: Journal Article
• Authors: Nakagami, Gojiro; Minematsu, Takeo; Morohoshi, Tomohiro; Yamane, Takumi; Kanazawa, Toshiki; Huang, Lijuan; Asada, Mayumi; Nagase, Takashi; Ikeda, Shin-ichi; Ikeda, Tsukasa; Sanada, Hiromi
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 79:Issue 10(2015)
• Page Start: 1719
• Page End: 1724
• Publication Date: 2015-10-03
• Subjects: inflammation -- 3-Oxododecanoyl homoserine lactone -- quorum sensing -- wound infection; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2015.1056509
• Languages: English
• ISSNs: 0916-8451

Abstract

Abstract: Quorum sensing is a cell-to-cell communication mechanism, which is responsible for regulating a number of bacterial virulence factors and biofilm maturation and therefore plays an important role for establishing wound infection. Quorum-sensing signals may induce inflammation and predispose wounds to infection by Pseudomonas aeruginosa ; however, the interaction has not been well investigated. We examined the effects of the P. aeruginosa las quorum-sensing signal, N-3-oxo-dodecanoyl homoserine lactone (3OC12-HSL), on matrix metalloproteinase (MMP) 9 expression in Rat-1 fibroblasts. 3OC12-HSL upregulated the expression of the MMP9 gene bearing an activator protein-1 (AP-1) binding site in the promoter region. We further investigated the mechanism underlying this effect. c - Fos gene expression increased rapidly after exposure to 3OC12-HSL, and nuclear translocation of c-Fos protein was observed; both effects were reduced by pretreatment with an AP-1 inhibitor. These results suggest that 3OC12-HSL can alter MMP9 gene expression in fibroblasts via the AP-1 signaling pathway. Graphical abstract: : Pseudomonas aeruginosa quorum-sensing signaling molecule induces matrix metalloproteinase 9 expression via the AP1 pathway in rat fibroblasts