Our group is involved in the analysis of host-pathogen interactions during fungal infection. We mainly use Candida albicans as model organism to explore fungal pathogenesis. C. albicans is a dimorphic yeast that frequently inhabits the gastrointestinal and vaginal tract in humans; however, under circumstances that result in impaired host immunological responses (such as those that result from HIV infection or treatment with immune suppressors) it is able to gain access to different target organs and generate diseases collectively called candisiasis. It is therefore, an opportunistic fungal pathogen and probably the best established model of fungal pathogenesis.

Our work mainly focuses on the role that MAP kinase signal transduction pathways play in this microbe; these cascades rely on phosphorylation for the transmission of an environmental-generated signal to the nucleus where a transcriptional response is developed allowing adaptation to the new conditions.  We are interested determining the specificity of the stimuli, the responses generated and the interactions among these routes. We want to determine the consequences of their activation, with special emphasis in their role in cell wall biosynthesis and dimorphism, as both processes are essential to the cell. A better understanding of this complex system may be exploited for the design of new and novel antifungals.

Experimental approaches and methodologies used in our research comprise molecular genetics, biochemistry, cell biology, genome wide strategies (transcriptomal and proteomic) and experimental infection in mice.

Recently, we are using genetically modified strains disrupted in genes essential to pathogenesis to understand the mechanisms used by the immune system to control Candida infections. We are determining the key components (receptors and/or cytokines) that influence the decision of the host towards control (commensalism) or susceptibility to invasion (disease). In particular, we are paying attention to the role of dendritic cells and neutrophils as key cells that determine influence antigen presentation and cell killing (respectively) and therefore progression or control of the disease. We are also using model of commensalism in mice to define the role of certain host specific genes in susceptiblity to infection. We are finally interested in how to exploit colonization in benefit of human health.