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Pseudomonas aeruginosa Lipopolysaccharide Induction of Keratinocyte Proliferation, NF-B, and Cyclin D1 Is Inhibited by Indomethacin¹

Diego Preciado^*, Emiro Caicedo^*, Rajat Jhanjee^*, Rob Silver^*, George Harris^*, Steven K. Juhn^*, Dan I. Choo and Frank Ondrey^2,*

^* Department of Otolaryngology-Head and Neck Surgery, Molecular Oncology Program, University of Minnesota, Minneapolis, MN 55455; and Center for Hearing and Deafness Research, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229

NF-B is activated during acute inflammatory states as well as in other injury response disease states. Several pathologic states in squamous tissue injury response are characterized by increased squamous proliferation. This study was performed to investigate the hypothesis that Pseudomonas aeruginosa LPS is able to activate a proliferative phenotype in squamous cells via NF-B induction and that this NF-B-mediated response may be abrogated with the classic anti-inflammatory agent indomethacin. EMSA, luciferase reporter gene experiments, Western blots, and cellular proliferation assays were performed in normal and transformed human keratinocytes after stimulation with P. aeruginosa LPS. EMSA and luciferase reporter gene assays showed a 3- to 5-fold induction of active NF-B in human keratinocyte cell lines after stimulation with P. aeruginosa LPS. The stimulation correlated with significantly increased cellular proliferation. As one potential mechanism for this increase in proliferation, an NF-B-specific activation of cyclin D1 was observed. Both the NF-B induction and proliferation response were inhibited with indomethacin and in dominant negative stable transfection clones. P. aeruginosa LPS activates proliferation of human keratinocytes, potentially through the induction of NF-B and cyclin D1. These findings suggest that bacterial components can contribute to proliferative disease states in squamous epithelium through NF-B activation.

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