title: Candida-induced oral epithelial cell responses.
abstract: OBJECTIVE
  Oropharyngeal candidiasis (OPC), caused by Candida albicans, is the most common oral infection in HIV(+) persons. Oral epithelial cells are considered important for innate host defense against OPC with production of cytokines in response to C. albicans and the ability to inhibit Candida growth in vitro. The purpose of this study was to determine if Candida similarly induces cytokines by oral epithelial cells from HIV(+) persons, including those with OPC, as well as to determine if cytokines can influence the oral epithelial cell anti-Candida activity.
  
  
  METHODS
  Supernatants from oral epithelial cells from HIV(+) persons with and without OPC cultured with Candida were evaluated for cytokines by ELISA, or cytokines were added to the standard growth inhibition assay using epithelial cells from HIV(-) persons.
  
  
  RESULTS
  Results showed low Candida-induced epithelial cell cytokine production from HIV(+) persons, but with some elevated proinflammatory cytokines (TNF-alpha, IL-6) in those with OPC compared to those without OPC. The addition of specific proinflammatory or Th cytokines had no effect on oral epithelial cell anti-Candida activity in healthy HIV(-) persons.
  
  
  CONCLUSIONS
  These results suggest that oral epithelial cells from HIV(+) persons can contribute at some level to the oral cytokine milieu in response to Candida during OPC, but that cytokines do not appear to influence oral epithelial cell anti-Candida activity.
authors.affiliation: Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center and School of Dentistry, New Orleans, LA, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Lilly
authors.forename: J E
authors.initials: JE
authors.lastname: Leigh
authors.forename: S H
authors.initials: SH
authors.lastname: Joseph
authors.forename: P L
authors.initials: PL
authors.lastname: Fidel
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000276:immunology / Q000382:microbiology*; D002176:Candida albicans / Q000254:growth & development*; D002180:Candidiasis, Oral / Q000276:immunology / Q000382:microbiology / Q000821:virology*; D015331:Cohort Studies; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D006678:HIV / Q000254:growth & development*; D015658:HIV Infections / Q000276:immunology / Q000382:microbiology* / Q000821:virology; D006801:Humans; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016207:Cytokines