title: Differential expression of Toll-like receptors in chronic hyperplastic candidosis.
abstract: BACKGROUND
  The first step in the host defense against oral candidosis is the recognition of Candida albicans through a set of germ-encoded pathogen recognition receptors, e.g. Toll-like receptors (TLRs). In man, 10 types of such receptors have been identified so far, of which only TLR2, TLR4, and TLR6 have been linked to mediating candidal ligands, e.g. zymosan.
  
  
  METHODS
  Biopsies from patients with chronic hyperplastic candidosis (n = 5), leukoplakia (n = 5), and healthy mucosa (n = 5) were immunohistochemically stained with antibodies to the TLRs (TLR1 to TLR9) to distinguish and compare the staining patterns of the epithelial layer in the three categories of tissues.
  
  
  RESULTS
  On analysis, the epithelium of all tissues was divided into three layers: basal, middle, and superficial. Two of the five chronic hyperplastic candidosis sections showed high numbers of hyphae compared to yeasts, which paralleled a decrease in the expression of TLR2 and an increase in the staining intensity of TLR4. Leukoplakia and healthy tissue sections demonstrated stronger immunostaining of TLRs, except TLR9 which showed weaker staining in some sections of the former, and in the basal layers of some sections of the latter.
  
  
  CONCLUSIONS
  This study supports the concept of negative regulation of TLRs that are either ligand-bound (e.g. in chronic hyperplastic candidosis), or not stimulated (in healthy tissue). It also augments the opinion that C. albicans, through its hyphae rather than blastospore, may utilize TLRs, i.e. TLR2, to evade the immune system of the host. Leukoplakia seems to be more immunologically alert, which reduces the chances of worsening the already-diseased tissue.
authors.affiliation: Department of Anatomy/Biomedicum, University of Helsinki, Helsinki, Finland. ahmed.ali@helsinki.fi
authors.forename: A
authors.initials: A
authors.lastname: Ali
authors.forename: S
authors.initials: S
authors.lastname: Natah
authors.forename: Y
authors.initials: Y
authors.lastname: Konttinen
mesh_terms: D002176:Candida albicans / Q000276:immunology; D002180:Candidiasis, Oral / Q000276:immunology*; D002908:Chronic Disease; D004848:Epithelium / Q000276:immunology; D006801:Humans; D006965:Hyperplasia; D025301:Hyphae / Q000276:immunology; D007972:Leukoplakia, Oral / Q000276:immunology; D009061:Mouth Mucosa / Q000276:immunology; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2 / Q000032:analysis; D051196:Toll-Like Receptor 3 / Q000032:analysis; D051197:Toll-Like Receptor 4 / Q000032:analysis; D051198:Toll-Like Receptor 5 / Q000032:analysis; D051216:Toll-Like Receptor 6 / Q000032:analysis; D051199:Toll-Like Receptor 7 / Q000032:analysis; D051200:Toll-Like Receptor 8 / Q000032:analysis; D051217:Toll-Like Receptor 9 / Q000032:analysis; D051193:Toll-Like Receptors / Q000032:analysis / Q000145:classification*
chemical_list: C495342:TLR2 protein, human; C495344:TLR3 protein, human; C495345:TLR4 protein, human; C495346:TLR5 protein, human; C495368:TLR6 protein, human; C495348:TLR7 protein, human; C495349:TLR8 protein, human; C495371:TLR9 protein, human; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051196:Toll-Like Receptor 3; D051197:Toll-Like Receptor 4; D051198:Toll-Like Receptor 5; D051216:Toll-Like Receptor 6; D051199:Toll-Like Receptor 7; D051200:Toll-Like Receptor 8; D051217:Toll-Like Receptor 9; D051193:Toll-Like Receptors