Contact of Chlamydophila pneumoniae with type II cell triggers activation of calcium-mediated NF-κB pathway

Nuclear factor-kappa B (NF-kappa B) plays an important role in inflammation, proliferation and regulation of 2 apoptosis. The purpose of the present study on type 11 cells was to investigate whether Chlamydophila pneumoniae contact induces (I) a Ca2+ release, that (II) disrupts F-actin/beta-tubulin cytoskeletal association with NF-kappa B/I kappa B alpha, leading to (III) a subsequent NF-kappa B activation. Incubation of rat type II pneumocytes with C. pneumoniae caused an intracellular calcium release within seconds. Confocal laser scanning microscopy (CLSM) revealed that bacterial contact with cell surface leads to a disappearance of the microvilli and disturbs the co-localization between F-actin and NF-kappa B (p65). Using semi-quantitative CLSM, we show that at 10-30 min I kappa B alpha was decreased and p65 or p50 was simultaneously translocated from cytoplasm to the nucleus, resulting in a 19-fold and 17-fold increase versus control cells. During this time no bacteria were internalized into type II cells. The pre-treatment of cells with BAPTA-AM inhibited C. pneumoniae -mediated calcium release. BA-PTA-AM or SN50 prevented the C pneumoniae -induced changes in F-actin cytoskeleton and inhibited NF-kappa B activation. Paclitaxel reduced C pneumoniae-mediated changes of beta-tubulin cytoskeleton and activation of NF-kappa B. These results suggest that calcium-mediated cytoskeleton reorganization is involved in C pneumoniae -induced NF-kappa B activation in type 11 cells. (c) 2004 Elsevier B.V. All rights reserved.