Investigation of Protein Kinase C-dependent Na+-K+-2Cl– cotransporter 1 Internalization During Candida albicans Infection in Madin-Darby Canine Kidney Cells

Faculty Sponsor

Dr. Patrice Bouyer

College

College of Arts & Sciences (CAS)

Department/Program

Biology

Presentation Type

Poster Presentation

Symposium Date

Summer 7-22-2026

Abstract

Invasive candidiasis is a fungal infection originating in the gastrointestinal tract caused by an overgrowth of Candida albicans. Before invading intestinal epithelial cells, C. albicans must overcome host defense mechanisms, including chloride (Cl⁻)-driven fluid secretion, a process facilitating the removal of pathogens from the intestinal lumen. Preliminary research demonstrates that C. albicans decreases basolateral Na⁺–K⁺–2Cl⁻ cotransporter (NKCC1) membrane expression, reducing fluid secretion necessary for mucosal defense and pathogen clearance. This study investigates whether C. albicans induces NKCC1 endocytosis by subverting the well-described PKC-dependent mechanism of NKCC1 internalization. Madin-Darby Canine Kidney (MDCK) cells stably expressing eGFP-NKCC1 were used as a model to study NKCC1 internalization during C. albicans infection. NKCC1 internalization was induced by treatment with the PKC activator phorbol 12-myristate 13-acetate (PMA). In contrast, treatment with Gö6850, a PKC inhibitor, resulted in a reduction of PMA-induced NKCC1 internalization. After 90 minutes of infection of MDCK cells with filamentous yeast, NKCC1 internalization was observed in some slides; however, this effect was not consistent across all slides. Treatment with Gö6850 reduced NKCC1 internalization during yeast infection in some cases, but this effect was variable and was not consistently observed in all slides. Further experimentation is necessary to assess whether or not C. albicans subverts PKC-mediated NKCC1 endocytosis.

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