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http://dx.doi.org/10.5352/JLS.2008.18.4.530

Effects of Pseudomonas fluorescens on Production of Several Inflammatory Mediators in the Human Alveolar Epithelial Cells.  

Yang, Hyun (Department of Microbiology and Immunology, Medical Research Institute, Pusan National University School of Medicine)
Ryoo, Jung-Min (Korea science academy)
Park, Seung-Hwan (Department of Microbiology and Immunology, Medical Research Institute, Pusan National University School of Medicine)
Choi, Hye-Jin (Department of Microbiology and Immunology, Medical Research Institute, Pusan National University School of Medicine)
Kim, Na-Yeon (Korea science academy)
Cho, Hyung-Hoon (Korea science academy)
Ahn, Jung-Hoon (Korea science academy)
Moon, Yu-Seok (Department of Microbiology and Immunology, Medical Research Institute, Pusan National University School of Medicine)
Publication Information
Journal of Life Science / v.18, no.4, 2008 , pp. 530-536 More about this Journal
Abstract
To investigate the molecular mechanism of the airway inflammation by Pseudomonas fluorescens, effects on the inflammatory mediators such as interleukin-8 (IL-8), cyclooxygenase-2 (COX-2), macophage inhibitory cytokine 1 (MIC-1) were assessed in the human alveolar epithelial cells. Exposure to P. fluorescens and its recombinant bacteria suppressed cellular viability in the A549 epithelial cells and pro-inflammatory cytokine interleukin-8 production. However, pro-inflammatory prostaglandin-producing COX-2 protein was not altered by P. fluorescens though its mRNA was slightly elevated. As the inhibitory cytokine for the pro-inflammatory mediators, MIC-1 expression was monitored in A549 cells. MIC-1 gene induction was not significantly enhanced but the protein processing was changed by exposure to P. fluorescens. Pro-protein form of MIC-1 (${\sim}40\;kD$) was cleaved into active form mature MIC-1 (${\sim}15\;kD$) and propeptide (${\sim}28\;kD$) by the bacteria exposure. MIC-1 activation can contribute to the suppression of cellular viability by P. fluorescens and can retard IL-8-induced monocyte recruitment. However, sustained activation of MIC-1 can mediate the tissue injury by P. fluorescens exposure.
Keywords
Pseudomonas fluorescens; airway inflammation; macophage inhibitory cytokine 1; interleukin-8; cyclooxygenase-2;
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