The opportunistic pathogen Candida albicans is a frequent inhabitant of the human gastrointestinal tract where it usually behaves as a harmless commensal. In this particular niche, it needs to adapt to the different micro environments that challenge its survival within the host. In order to determine those factors involved in gut adaptation, we have used a gastrointestinal model of colonization in mouse to trace the behaviour of fungal cells. We have developed a genetic labelling system based on the complementary spectral properties of the fluorescent proteins GFP and a new C. albicans codon-adapted RFP (dTOM2) that allow a precise quantification of the fungal population in the gut via standard in vitro cultures or flow cytometry. This methodology has allowed us to determine the role of the three MAP kinase pathways of C. albicans (mediated by the MAPK Mkc1, Cek1 or Hog1) in mouse gut colonization via competitive assays with MAPK pathway mutants and their isogenic wild type strain. This approach reveals the signalling through HOG pathway as a critical factor influencing the establishment of C. albicans in the mouse gut. Less pronounced effects for mkc1 or cek1 mutants were found, only evident after 2–3 weeks of colonization. We have also seen that hog1 mutants is defective in adhesion to the gut mucosa and sensitive to bile salts. Finally, we have developed a genetic strategy for the in vivo excision (tetracycline-dependent) of any specific gene during the course of colonization in this particular niche, allowing the analysis of its role during gut colonization.

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Candida albicans is a common resident of the oral cavity, GI tract and vagina in healthy humans where it establishes a commensal relationship with the host. Colonization of the gut, which is an important niche for the microbe, may lead to systemic dissemination and disease upon alteration of host defences. Understanding the mechanisms responsible for the adaptation of C. albicans to the gut is therefore important for the design of new ways of combating fungal diseases. In this review we discuss the available models to study commensalism of this yeast, the main mechanisms controlling the establishment of the fungus, such as microbiota, mucus layer and antimicrobial peptides, and the gene regulatory circuits that ensure its survival in this niche.

PURPOSE Although dental impression disinfection is determinant to reduce the cross-infection risk, some studies have shown that, in real practice, the disinfection procedures vary considerably. Thus, the aim of this study was to evaluate the antimicrobial effectiveness and the impact on the dimensional stability of addition silicone' impressions of water wash and the most clinically used disinfection solutions: 3% hydrogen peroxide, commercial disinfectant MD520 (Durr) and 1% and 5.25% sodium hypochlorite. MATERIALS AND METHODS For this investigation, dental impressions were taken on 16 volunteer dental students. The antimicrobial effectiveness of each procedure was evaluated by pour plate method. The dimensional stability was evaluated using a standardized stainless-steel model, according to ANSI/ADA nº19 specification. RESULTS The study results showed that water wash does not alter the dimensional stability of addition silicone impressions but doesn't reduce the microbial load of the material ( P >.05). On the other hand, addition silicone disinfection by immersion with 3% hydrogen peroxide, MD520 (Durr), or sodium hypochlorite at 1% and 5.25% does not alter the dimensional stability significantly but reduces > 99.9% of the microbial load of the impressions ( P <.001). CONCLUSION Addition silicone impressions should always be disinfected after water wash in order to reduce effectively the cross-infection risk. All disinfectants tested showed high antimicrobial efficiency without significant changes in three-dimensional shape of impressions. Hydrogen peroxide and sodium hypochlorite are of particular importance because are easily accessible in dental setting. The less explored hydrogen peroxide could be a valuable alternative for silicone impressions disinfection.

Cek2 has a cryptic role in cell-wall biogenesis and its role is not entirely redundant to Cek1.

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The overproduction of Cat1 protects against oxidants, phagocytes and certain antifungals at subinhibitory concentration but does not increase virulence in a systemic infection mouse model.

The cell cycle is the sequential set of events that living cells undergo in order to duplicate. This process must be tightly regulated as alterations may lead to diseases such as cancer. The molecular events that control the cell cycle are directional and involve regulatory molecules such as cyclins and cyclin-dependent kinases (CDKs). The budding yeast Saccharomyces cerevisiae has become a model to study this complex system since it shares several mechanisms with higher eukaryotes. Signal transduction pathways are biochemical mechanisms that sense environmental changes and there is recent evidence that they control the progression through the cell cycle in response to several stimuli. In response to pheromone, the budding yeast arrests the cell cycle in the G1 phase at the START stage. Activation of the pheromone response pathway leads to the phosphorylation of Far1, which inhibits the function of complexes formed by G1 cyclins (Cln1 and Cln2) and the CDK (Cdc28), blocking the transition to the S phase. This response prepares the cells to fuse cytoplasms and nuclei to generate a diploid cell. Activation of the Hog1 MAP kinase in response to osmotic stress or arsenite leads to the transient arrest of the cell cycle in G1 phase, which is mediated by direct phosphorylation of the CDK inhibitor, Sic1, and by downregulation of cyclin expression. Osmotic stress also induces a delay in G2 phase by direct phosphorylation of Hsl7 via Hog1, which results in the accumulation of Swe1. As a consequence, cell cycle arrest allows cells to survive upon stress. Finally, cell wall damage can induce cell cycle arrest at G2 via the cell integrity MAPK Slt2. By linking MAPK signal transduction pathways to the cell cycle machinery, a tight and precise control of the cell division takes place in response to environmental changes. Research into similar MAPK-mediated cell cycle regulation in the opportunistic pathogen Candida albicans may result in the development of new antifungal therapies.