Interaction of the mucosal barrier with accessory immune cells during fungal infection

Günther Weindl, Jeanette Wagener, Martin Schaller

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The mucosal epithelium is of central importance in host defence and immune surveillance, as it is the primary cell layer that initially encounters environmental microorganisms. Induction of antifungal innate immune responses depends on recognition of fungal components by host pattern recognition receptors. Members of the Toll-like receptor family have emerged as key sensors that recognize fungal pathogens and trigger defence responses. During oral infection with the fungal pathogen Candida albicans, a large number of cytokines is secreted by oral epithelial cells, which in turn activate myeloid cells in the submucosal layers to clear the invading pathogen. Recent data provide novel insights into the complex molecular mechanisms of innate immune responses initiated by cooperation between epithelial cells and neutrophils. In this review, we discuss the role of epithelial TLRs and how the immunological crosstalk between C. albicans-infected oral epithelium and neutrophils protects the mucosal surface from fungal invasion and cell injury.
Original languageEnglish
Pages (from-to)431-435
Number of pages5
JournalInternational Journal of Medical Microbiology: IJMM
Volume301
Issue number5
DOIs
Publication statusPublished - Jun 2011

Fingerprint

Mycoses
Candida albicans
Innate Immunity
Neutrophils
Epithelium
Epithelial Cells
Fungal Structures
Pattern Recognition Receptors
Toll-Like Receptors
Myeloid Cells
Cytokines
Wounds and Injuries

Keywords

  • Candida albicans
  • candidiasis, oral
  • cytokines
  • epithelial cells
  • humans
  • immunity, mucosal
  • neutrophils
  • toll-like receptors

Cite this

Interaction of the mucosal barrier with accessory immune cells during fungal infection. / Weindl, Günther; Wagener, Jeanette; Schaller, Martin.

In: International Journal of Medical Microbiology: IJMM, Vol. 301, No. 5, 06.2011, p. 431-435.

Research output: Contribution to journalArticle

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