Colonization in the intestinal tract requires coordinated communication between the opportunistic fungal pathogen Candida albicans and the host. C57BL/6 mice and Swiss Webster mice were animal models used to examine the requirements for colonization. The involvement of a putative transcription factor, EFH1, during commensal colonization was studied. Other genetic factors such as Chromosome 1 copy number, auxotrophy, hyphal specific genes and transcription factors were examined.

The C57BL/6 inbred strain of mouse and Swiss Webster outbred strain of mouse were found to respond differently to C. albicans. C57BL/6 mice were less sensitive to the titration of C. albicans in the intestines. In contrast to observations in Swiss Webster mice, the efh1 null mutant did not hypercolonize C57BL/6 mice and the EFH1 overexpressing strain did not hypocolonize. Inoculation of Toll-like receptor 2 (TLR2) knockout mice in the C57BL/6 background did not affect the colonization of C. albicans, which suggested that TLR2 does not play a significantly detectable role in colonization.

Various assays further elucidated the role of EFH1. The EFH1 overexpressing strain was found to be resistant to 40 µg/ml Calcofluor white and sensitive to 0.1% SDS and 1.5M NaCl. The efh1 null mutant was sensitive to 500 µg/ml Congo red. Under embedded filamentation conditions, the EFH1 overexpressing strain was hyperfilamentous. It seemed to also be defective in forming biofilms. The aerobically grown EFH1 overexpressing cells had a similar growth phenotype compared to the wildtype strain, while exhibiting a poor growth phenotype under anaerobic conditions. These experiments allowed for explanation of the poor colonization observed in Swiss Webster mice by the EFH1 overexpressing strain.