Pathogenicity mechanisms at the mucosal interphase

In vitro translocation model simulates the intestinal epithelial barrier

In the healthy host, certain Candida species live as harmless commensals on mucosal surfaces like the oral, vaginal or intestinal mucosa. Under predisposing conditions, these Candida species growing on the oral or vaginal mucosa can cause tissue damage associated with induction of inflammation, immunopathology, and disease that significantly impacts quality of life.

When immune defense and microbiota are compromised in hospitalized patients or when the intestinal barrier is disturbed, fungal populations of the intestinal tract can invade the intestinal epithelial barrier and translocate into the bloodstream. From here, the fungus can infect virtually all organs and cause systemic fungal infection. Our aim is to elucidate which fungal and host factors mechanistically allow fungal adhesion to, invasion into, and damage of epithelial cells as well as translocation through intestinal barriers and invasion of host tissues.

To unravel host-pathogen interactions at the epithelial interface for C. albicans, but also C. glabrata and the newly emerged, multidrug-resistant species C. auris we are using in vitro infection models, genome-wide dual-species transcription profiling techniques, and fungal gene deletion strains.

Staff

Stefanie Allert
Lydia Kasper
Jakob Sprague

Publications

Dalle F, Wächtler B, L'Ollivier C, Holland G, Bannert N, Wilson D, Labruère C, Bonnin A, Hube B (2010) Cellular interactions of Candida albicans with human oral epithelial cells and enterocytes. Cell Microbiol 12(2), 248-271.
Wilson D, Thewes S, Zakikhany K, Fradin C, Albrecht A, Almeida R, Brunke S, Grosse K, Martin R, Mayer F, Leonhardt I, Schild L, Seider K, Skibbe M, Slesiona S, Waechtler B, Jacobsen I, Hube B (2009) Identifying infection-associated genes of Candida albicans in the postgenomic era. FEMS Yeast Res 9(5), 688-700. (Review)
Hube B (2004) From commensal to pathogen: stage- and tissue-specific gene expression of Candida albicans. Curr Opin Microbiol 7(4), 336-341. (Review)

Funding