Furthermore, ginseng could clearly also facilitate swimming

of the mucoid PDO300. As expected, the fliM mutant did not show any swimming motility in either condition (Fig. 4b). Twitching motility is caused by type IV pili-mediated bacterial translocation on a solid surface. Therefore, a pilA mutant was used as a negative control (Fig. 4c). Ginseng clearly induced twitching motility of both PAO1 and PDO300. The twitching motility of PAO1 was activated more than that of PDO300. The phagocytosis rate and index are expressed as Median (range) in the study. Twenty-four hours after intratracheal challenge, no significant differences Selleckchem LY2109761 were seen in both the phagocytosis rate and index between the PAO1-filM control and ginseng-treated groups (P>0.27 and >0.8). However, in the PAO1-infected animals, ginseng-treated BAL phagocytes showed a significantly higher phagocytosis rate (P=0.0004) and index (P<0.01) compared with the control animals (Fig. 5a and b). The biofilm mode of growth of P. aeruginosa in CF airways is associated with significant tolerance to antibiotics and the immune responses (Stewart & Costerton, 2001; Høiby et al., 2010). Biofilm formation of P. aeruginosa requires both type IV pili and flagella-mediated

motility (O’Toole & Kolter, 1998). More recently, type IV pili (but not the pili-associated motility) were shown to be required MEK inhibitor for interactions with extracellular DNA during the development of mature P. aeruginosa biofilm structures (Barken et al., 2008). In fact, excess twitching motility leads to a reduction of biofilm formation by P. aeruginosa (Singh et al., 2002). In contrast to twitching motility, flagella-mediated motility is required for the development of mature P. aeruginosa biofilm structures (Barken et al., 2008). The present study shows that ginseng does not inhibit the growth of P. aeruginosa (Fig. 1), but it prevents the efficient development of P. aeruginosa

biofilms in vitro (Fig. 2). Furthermore, preformed 7-day-old biofilms, including almost mucoid and nonmucoid laboratory strains and a clinical isolate, are almost completely dispersed within 24 h after exposure to ginseng extracts (Fig. 3). We have observed extensive cell movement in the microcolonies of biofilms treated with ginseng extracts (data not shown), which may result in cells migrating out of the preformed biofilms in accordance with the results from the swimming and twitching tests (Fig. 4b and c). These results indicate that flagellum-mediated swimming motility is not required for P. aeruginosa biofilm structure development. The presence of several dead bacterial cells in the biofilms after exposure to ginseng extract suggests that ginseng extract also activates apoptosis-like mechanisms in the biofilm cells (Fig. 3). We have also demonstrated in another study that such effects of ginseng are not dominated by ginseng saponins (data not shown).