At the investigated early time point of cold adaptation, the transcriptome is reprogrammed in almost all functional categories, but the protein profile has still not adapted to the change of living conditions in the cold. S.F. received a predoctoral

stipend from the DFG-supported IRTG 653 ‘Pseudomonas: Pathogenicity and Biotechnology’. Financial support was provided by BMBF within the framework of the SysMO consortium, part PSYSMO ‘Towards a quantum increase in the performance of P. putida as the cell factory of choice for white biotechnology,’ project 3: Key determinants of abiotic stress response of P. putida KT2440′. Table S1. Genes that were PD-0332991 chemical structure detected to be differentially expressed upon cold shock according to Illumina cDNA sequencing. Table S2. Calculated SD of biological replicates at 10 °C. Table S3. Calculated SD of biological Androgen Receptor Antagonist molecular weight replicates at 30 °C. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing

material) should be directed to the corresponding author for the article. “
“Saccharomyces boulardii is a probiotic strain that confers many benefits to human enterocolopathies and is used against a number of enteric pathogens. Candida albicans is an opportunistic pathogen that causes intestinal infections in immunocompromised patients, and after translocation into the bloodstream, is responsible for serious systemic candidiasis. In this study, we investigated the influence of S. boulardii cells and its culture extract 3-mercaptopyruvate sulfurtransferase on C. albicans adhesion to Caco-2 and Intestin 407 cell lines. We also tested the proinflammatory IL-1β, IL-6 and IL-8 cytokine expression by C. albicans-infected Caco-2 cells, using real-time RT-PCR. We found that both S. boulardii and its extract significantly inhibited C. albicans adhesion to epithelial cell lines. The IL-8 gene expression by C. albicans-infected

Caco-2 cells was suppressed by the addition of S. boulardii extract. Our results indicate that S. boulardii affects C. albicans adhesion and reduces cytokine-mediated inflammatory host response. The natural microbiota and the surface of the intestinal mucosa interact with each other and act as a barrier to prevent colonization of the intestine surface by pathogenic microorganisms. Pathogen infections induce the secretion of many cytokines by epithelial cells, including tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-4, IL-6 and IL-8 (Kagnoff & Eckmann, 1997; Xing et al., 1998; Apte & Voronov, 2002). Candida albicans is the most common opportunistic fungal pathogen isolated from the human body. It possesses many virulence factors such as adhesion, biofilm formation and morphological transformation. The first and necessary step in infection is adherence.