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Characterization of Candida parapsilosis infection of an in vitro reconstituted human oral epithelium
Author(s) -
Silva Sónia,
Henriques Mariana,
Oliveira Rosário,
Azeredo Joana,
Malic Sladjana,
Hooper Samuel J.,
Williams David W.
Publication year - 2009
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2009.00677.x
Subject(s) - candida parapsilosis , biology , microbiology and biotechnology , candida albicans , epithelium , virulence , corpus albicans , oral mucosa , gene , anatomy , biochemistry , genetics
Oral candidosis is a common problem in immunocompromised patients, and whilst Candida albicans is regarded as the principal cause of infection, other non‐ Candida albicans Candida (NCAC) species are increasingly being recognized as human pathogens. Relatively little is known about the virulence factors associated with NCAC species, and the aim of this study was to use a reconstituted human oral epithelium (RHOE) to examine epithelial infection with Candida parapsilosis . Strains originating from the oral and vaginal mucosa and from the urinary tract were all shown to colonize RHOE in a strain‐dependent manner. Strain differences were found in the colonizing morphology and in the extent of invasion of the RHOE. Low invasion of RHOE was detected for strains after 12 h, whereas extensive tissue damage was evident after 24 h when assessed using histological examination and lactate dehydrogenase activity determination. Tissue damage was reduced in the presence of pepstatin A, although C. parapsilosis invasion of the tissue was not inhibited. Real‐time polymerase chain reaction of secreted aspartyl proteinase ( SAP) genes ( SAPP1–3 ) showed that expression was strain dependent, with an increased expression generally occurring for Candida infecting RHOE compared with planktonic equivalents. In summary, C. parapsilosis was not highly invasive of RHOE but did induce significant tissue damage, which could relate to specific SAP gene expression.