title: Pathological analysis of the Candida albicans-infected tongue tissues of a murine oral candidiasis model in the early infection stage.
abstract: OBJECTIVE
  The early pathological process of Candida infection and immunological responses in tongues of the mice with experimental oral candidiasis was analysed.
  
  
  METHODS
  CD-1 mice, pretreated by prednisolone were orally inoculated with Candida albicans. Symptoms were monitored by measuring the area of white tongue coating and number of viable Candida cells in oral cavity. The histopathological analysis was carried by PAS-stain and immunofluorescent staining. IL-4, IL-12p70, IFN-γ, TNF-α in recovered from the homogenates of the tongues were measured by ELISA.
  
  
  RESULTS
  The fungus invaded the tongue surface of the mice and white patches developed within 24h after inoculation. Histopathological examination indicated the presence of local acute inflammation in superficial tissues of tongues covered by mycelium of C. albicans. Pathological exacerbation was observed from 24 to 48 h after the inoculation and from then the symptoms of oral candidiasis appeared to move into the recovery phase. Inflammatory cells mainly consisting of neutrophils was accumulated and located under the lesions covered by Candida-hyphae. An increase in IL-12p70 and IFN-γ in tongue homogenates was observed at 48 h after inoculation.
  
  
  CONCLUSIONS
  The worst condition in the pathological process in experimental oral candidiasis was found 48 h after C. albicans inoculation. When the surface of the Candida-inoculated tongues was covered with Candida-hyphae, a dense accumulation of neutrophils was observed under the lesions and homogenates of the tongues contained increased levels of IL-12p70 and IFN-γ. These suggested that local pathological condition of Candida-infected tongues may be affected by neutrophils accumulation and increased levels of some cytokines.
authors.affiliation: Department of Oral and Maxillofacial Surgery, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo, Japan. masashiokada1979@gmail.com
authors.forename: Masashi
authors.initials: M
authors.lastname: Okada
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Hisajima
authors.forename: Hiroko
authors.initials: H
authors.lastname: Ishibashi
authors.forename: Takahiro
authors.initials: T
authors.lastname: Miyasaka
authors.forename: Shigeru
authors.initials: S
authors.lastname: Abe
authors.forename: Tazuko
authors.initials: T
authors.lastname: Satoh
mesh_terms: D000818:Animals; D002180:Candidiasis, Oral / Q000473:pathology*; D015169:Colony Count, Microbial; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000032:analysis*; D018664:Interleukin-12 / Q000032:analysis*; D015847:Interleukin-4 / Q000032:analysis*; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000502:physiology*; D011239:Prednisolone; D014059:Tongue / Q000737:chemistry / Q000382:microbiology / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma; D011239:Prednisolone