The course of infectious disease critically depends on host cell mechanisms including transport. Recent evidence highlights the significance of CFTR as a receptor for Pseudomonas aeruginosa. CFTR seems to be involved in the internalization of P. aeruginosa and the induction of apoptosis of the host cell during the course of infection (1-3). Internalization requires lipid rafts and the transformation of those rafts into large ceramide-enriched membrane platforms (1, 2) that initiate intracellular signalling including the activation of src like kinases (3). Apoptosis of infected cells is mediated by a stimulation of the CD95/CD95 ligand system (4), which has been shown to result in a src like kinase-dependent activation of outwardly rectifying Cl- channels in lymphocytes (5). Exposure of Chang cells to P. aeruginosa indeed leads to activation of outwardly rectifying Cl- channels, an effect, however, not required for induction of apoptosis (6). Lack of CD95 or of its ligand abrogates host cell apoptosis in vitro and leads to lethal lung infection in vivo (2, 4, 7). Thus, pathogen induced host cell apoptosis is an important defence mechanism against infection with P. aeruginosa. Further evidence points to a role of the serum and glucocorticoid inducible kinase SGK1 in cystic fibrosis and lung infection. SGK1 is known to upregulate the epithelial Na+ channel ENaC (8-10) and the Cl- channel CFTR (11). The expression of SGK1 is heavily upregulated in fibrosing tissue such as diabetic nephropathy (9), liver scirrhosis (12), Crohn’s disease (13), and lung fibrosis (14). Most recent observations indicate that the kinase may indeed be required for the induction of fibrosis. In conclusion, host cells play a decisive role in the course of lung infection. The mechanisms triggered in host cells include activation of kinases and subsequent stimulation of ion channels. Those mechanisms may participate in the triggering of pathogen internalization, host cell apoptosis and/or enhanced matrix protein deposition.