, 1997). In particular, the molecular weight of this Kwkt killer protein differs from the weight of the other investigated zymocins that are active against Brettanomyces/Dekkera (De Ingeniis et al., 2009; Santos et al., 2009). Moreover, we demonstrated the capability of Kwkt to control both the growth and 4-ethyl phenol production of spoilage D. bruxellensis yeast during wine fermentation. The data obtained in this study thus strongly indicate that Kwkt can be used as a natural antimicrobial agent for the biocontrol of such sensitive spoilage yeasts as Brettanomyces/Dekkera

under winemaking conditions at low concentrations. Other killer toxins such as PMKT2 produced by P. selleck compound membranifaciens (Santos et al., 2009) and PiKt produced by P. anomala (Comitini et al., 2004a; De Ingeniis et al., 2009) have also been found to be active against Dekkera/Brettanomyces under winemaking conditions. Thus, these bioactive compounds could be considered a valid alternative to chemical biocides or other physical treatments. The use of killer toxins in winemaking to control potential spoilage yeasts has been reported previously (Ciani & Fatichenti, 2001; Comitini & Ciani, 2010) for other potential spoilage yeasts, indicating that this environment supports the killing action of the toxins. In this context, use of killer yeasts or their killer

toxin Selleck CHIR99021 could be a profitable way to avoid the presence and activity of undesirable microorganisms. The authors would like to thank Chris Suplatast tosilate Berrie for critical appraisal of

the manuscript. “
“The Gram-negative bacterium Legionella pneumophila is an intracellular parasite of amoebae and an accidental human pathogen that causes a noncommunicable atypical pneumonia known as Legionnaires’ disease (LD). In some mammalian cells (e.g. HeLa), L. pneumophila follows a biphasic developmental cycle, differentiating between a replicative form that actively multiplies intracellularly, and a mature infectious form (MIF) that emerges as progeny. To date, it is not known whether the L. pneumophila progenies that emerge from amoebae and human macrophages reach similar developmental stages. Here, we demonstrate that in relation to the fully differentiated and highly infectious MIFs that emerge from amoebae, the L. pneumophila progeny that emerges from macrophages is morphologically undifferentiated, less resistant to antibiotics and less able to initiate infections. However, the L. pneumophila progeny from macrophages did not show any defects in intracellular growth. We thus concluded that macrophage infection with L. pneumophila yields a low number of bona fide MIFs. Because MIFs are the transmissive forms of L. pneumophila produced in vivo, our results showing that they are not efficiently produced in cultured macrophages provide an initial insight into why LD is not communicable.