Vulvovaginal candidiasis in a murine model of diabetes emphasizing the invasive ability of etiological agents

Future Microbiol. 2020 Jul:15:1001-1013. doi: 10.2217/fmb-2019-0223. Epub 2020 Aug 19.

Abstract

Aim: To compare the pathogenesis of vulvovaginal candidiasis by three Candida species in diabetic mice. Materials & methods: Estrogenized and diabetic mice were challenged with C. albicans, C. tropicalis and C. glabrata. Results: Diabetic animals infected with C. albicans and C. tropicalis maintained the highest fungal burden, despite of high levels of proinflammatory cytokines (IL-6 and TNF-α), respectively. For C. glabrata, the results were similar in diabetic and nondiabetic groups. Conclusion:C. tropicalis was as invasive as C. albicans, and both were more effective than C. glabrata. This ability was attributed to filamentation, which may be stimulated by glucose levels from vaginal fluid. In addition, the high burden may be attributed to the apparent immunological inefficiency of the diabetic host.

Keywords: Candida sp.; diabetes mellitus; etiopathogenesis; murine model; vulvovaginal candidiasis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Candida albicans / genetics
  • Candida albicans / isolation & purification
  • Candida albicans / physiology*
  • Candida glabrata / genetics
  • Candida glabrata / isolation & purification
  • Candida glabrata / physiology*
  • Candida tropicalis / genetics
  • Candida tropicalis / isolation & purification
  • Candida tropicalis / physiology*
  • Candidiasis, Vulvovaginal / etiology
  • Candidiasis, Vulvovaginal / genetics
  • Candidiasis, Vulvovaginal / metabolism
  • Candidiasis, Vulvovaginal / microbiology*
  • Diabetes Complications / etiology
  • Diabetes Complications / genetics
  • Diabetes Complications / metabolism
  • Diabetes Complications / microbiology*
  • Disease Models, Animal
  • Female
  • Humans
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Mice
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • Tumor Necrosis Factor-alpha