Molecular characterization of Legionella pneumophila-induced interleukin-8 expression in T cells

• DOI: 10.1186/1471-2180-10-1
• Publication Date: 2010-01-05T19:15:05Z
• Authors: Reika Takamatsu; Hiromitsu Teruya; Eriko Takeshima; Chie Ishikawa; Kunihiro Matsumoto; Naofumi Mukaida; Jian-Dong Li; Klaus Heuner; Futoshi Higa; Jiro Fujita; Naoki Mori
• Keywords: Flagellin; Legionella

Legionella pneumophila is the causative agent of human Legionnaire's disease. During infection, bacterium invades macrophages and lung epithelial cells, replicates intracellularly. However, little known about its interaction with T cells. We investigated ability L. to infect stimulate production interleukin-8 (IL-8) in The objective this study was assess whether interferes immune system by interacting infecting cells.Wild-type flagellin-deficient Legionella, but not lacking a functional type IV secretion Dot/Icm, replicated On other hand, wild-type Dot/Icm-deficient or heat-killed induced IL-8 expression. activated an promoter through NF-kappaB AP-1 binding regions. Wild-type NF-kappaB, p38 mitogen-activated protein kinase (MAPK), Jun N-terminal (JNK), transforming growth factor beta-associated 1 (TAK1). Transfection dominant negative mutants IkappaBalpha, IkappaB kinase, NF-kappaB-inducing TAK1, MyD88, MAPK inhibited pneumophila-induced activation. Inhibitors MAPK, JNK blocked In addition, c-Jun, JunD, cyclic AMP response element protein, activating transcription 1, which are substrates JNK, bound site promoter.Taken together, flagellin-dependent activation as well AP-1, resulted presumably contributing