title: In vitro interactions of Candida parapsilosis wild type and lipase deficient mutants with human monocyte derived dendritic cells.
abstract: BACKGROUND
  Candida parapsilosis typically is a commensal of human skin. However, when host immune defense is compromised or the normal microflora balance is disrupted, C. parapsilosis transforms itself into an opportunistic pathogen. Candida-derived lipase has been identified as potential virulence factor. Even though cellular components of the innate immune response, such as dendritic cells, represent the first line of defense against invading pathogens, little is known about the interaction of these cells with invading C. parapsilosis. Thus, the aim of our study was to assess the function of dendritic cells in fighting C. parapsilosis and to determine the role that C. parapsilosis-derived lipase plays in the interaction with dendritic cells.
  
  
  RESULTS
  Monocyte-derived immature and mature dendritic cells (iDCs and mDCs, respectively) co-cultured with live wild type or lipase deficient C. parapsilosis strains were studied to determine the phagocytic capacity and killing efficiency of host cells. We determined that both iDCs and mDCs efficiently phagocytosed and killed C. parapsilosis, furthermore our results show that the phagocytic and fungicidal activities of both iDCs and mDCs are more potent for lipase deficient compared to wild type yeast cells. In addition, the lipase deficient C. parapsilosis cells induce higher gene expression and protein secretion of proinflammatory cytokines and chemokines in both DC types relative to the effect of co-culture with wild type yeast cells.
  
  
  CONCLUSIONS
  Our results show that DCs are activated by exposure to C. parapsilosis, as shown by increased phagocytosis, killing and proinflammatory protein secretion. Moreover, these data strongly suggest that C. parapsilosis derived lipase has a protective role during yeast:DC interactions, since lipase production in wt yeast cells decreased the phagocytic capacity and killing efficiency of host cells and downregulated the expression of host effector molecules.
authors.affiliation: Department of Microbiology, University of Szeged, Közép fasor 52, H-6726 Szeged, Hungary.
authors.forename: István
authors.initials: I
authors.lastname: Nagy
authors.forename: Kata
authors.initials: K
authors.lastname: Filkor
authors.forename: Tibor
authors.initials: T
authors.lastname: Németh
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Hamari
authors.forename: Csaba
authors.initials: C
authors.lastname: Vágvölgyi
authors.forename: Attila
authors.initials: A
authors.lastname: Gácser
mesh_terms: D002175:Candida / Q000201:enzymology* / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000382:microbiology*; D006801:Humans; D008049:Lipase / Q000172:deficiency* / Q000378:metabolism*; D050296:Microbial Viability; D010587:Phagocytosis; D037521:Virulence Factors / Q000172:deficiency / Q000378:metabolism
chemical_list: D016207:Cytokines; D037521:Virulence Factors; D008049:Lipase