monocytogenes Trichostatin A research buy cytoxicity in protozoa. Our observations on the reduced growth of the hly gene deficient mutant in the co-culture with T. pyriformis compared to isogenic wild type bacteria are in line with a previous report that a hly gene deletion prevented L. monocytogenes from A. castellanii phagosome escaping [8]. Phagosome escaping is prerequisite for L. monocytogenes replication in mammalian but not insect cells [27]. It is not clear at present how the failure to escape the phagosome impairs intracellular growth in protozoan cells. However, the improved intracellular survival in synergy with rapid reduction of trophozoite concentration might be responsible

for the advantages that LLO exerts on bacterial survival in the presence of actively grazing protozoa. Considering the natural environment, LLO production seems to increase L. monocytogenes survival compared to non-haemolytic bacteria. Obtained results demonstrated higher counts for wild type L. monocytogenes than for the isogenic LLO deficient mutant during first days of co-cultivation supposing that wild type bacteria better survived upon initial interactions with the predator than non-haemolytic PF-01367338 ic50 counterparts. Furthermore, prolonged bacterial survival might be supported by bacterial maintenance in protozoan cysts forming due to LLO activity.

It see more is generally accepted that entrapped bacteria may benefit from the protective coat conferred by protozoan [28–30]. It has been demonstrated

previously that encysted bacteria could survive sewage water treatment, which is fatal to free living bacteria [31]. Survival HSP90 of human pathogens inside protozoan cysts was demonstrated previously for Vibrio cholerae, L. pneumophila, Mycobacterium spp and an avirulent strain of Yersinia pestis [32–34]. However, to our knowledge active stimulation of protozoan encystment by bacteria was demonstrated only in case of L. monocytogenes ([7]; and this work). Maintenance of pathogenic bacteria within cysts not only protects them from unfavorable environmental conditions but as well can preserve at the first stages of interactions with the macroorganism. That might be an important mechanism for bacterial spreading in the natural ecosystems when cyst protection not only supports pathogen survival in the hostile environment but as well increases its chance to multiply upon host invasion. Involvement of LLO in different aspects of interactions between L. monocytogenes and protozoa has a striking similarity with its multiples roles during infection in mammals. Phagosome membrane disruption is the major role for LLO in intracellular parasitism in mammalian cells [2, 14]. However, LLO input in L. monocytogenes virulence is not limited to phagosome escaping: LLO generates a calcium flux into cells, promotes bacterial invasion in certain epithelial cells, and causes apoptosis in dendritic cells and T lymphocytes [13, 17, 18].