Antagonistic effect of Candida albicans and IFN on E-cadherin expression and production by human primary gingival epithelial cells

Mahmoud Rouabhia, Abdelhabib Semlali, Julie Audoy, Witold Chmielewski Cellular Immunology, Volume 280, Issue 1, November 2012, Pages 6167 http://dx.doi.org/10.1016/j.cellimm.2012.11.008 Submitted by: Fallen Grace de la Paz 3BIO6

Mucosal candidiasis, especially the oropharyngeal type (OPC), is a common opportunistic infection in both immunocompromised and immunocompetent persons. The leading cause of candidiasis is Candida albicans, a commensal dimorphic yeast that colonizes up to 60% of normally healthy individuals. Symptomatic OPC appears under a number of predisposing conditions involving the adhesion, growth and invasion of C. albicans causing inflammation and tissue damage. C. albicans cells must migrate across epithelial layers leading to infect individual. The cells affected here are the primary gingival epithelial cells. To go through the tissues, Candida encounters multiple key proteins involved in cellcell contact including E-Cadherin. In the oral cavity, as a structural protein, E-cadherin has an epithelial attachment providing a structural barrier against noxious agents passing from the oral cavity into the tooth-supporting tissue . Abnormal degradation of E-cadherin may contribute to tissue weakness and susceptibility caused by C. albicans, provoking oral candidiasis.

Methodology
Oral Epithelial cell isolation and culture C. albicans growth Oral Epithelial cells culture in presence or not of C. albicans and IFN incubated at 4, 24, 48 hours RNA extraction and quantification Quantitative real time RT-PCR Western blotting and immunodetection of E-cadherin Immunohistochemistry
Primary antibody (E-cadherin) Goat anti-mouse IgG Optical microscopy

Results
E-cadherin mRNA expression in human oral epithelial cells was modulated by C.albicans. There was 50% reduction at 24 hours and 80% at 48 hours. E-cadherin production by human oral epithelial cells was decreased following culture infection with C. albicans IFN prevents the effect of C. albicans on E-cadherin gene expression and production

Conclusion
This study clearly demonstrated the damage caused by C. albicans to tissue integrity by inhibiting E-cadherin gene expression and protein production and deposition. We were also able to demonstrate the anti-candidal activity of IFN that prevents tissue structure contributing to the preservation of the barrier integrity against C. albicans invasion through Ecadherin secretion and deposition.