MUC16-dependent Renal Vascular Adhesion of Candida Promotes Tissue Invasion and Predicts Clinical Outcome in Candidemia.

Peter Williamson¹, Jin Qiu², Shellee Grim³, Guowu Hu², Yoon-Dong Park², Melissa Johnson⁴, Sunita Paaudel⁵, Troy Stevens⁵, John Perfect⁶, Visiliki Matzaraki⁷, Vinod Kumar⁸, Frank van de Veerdonk⁹, Mihai Netea⁹, Michail Lionakis¹⁰, Adebo Adebowale², Scott Filler¹¹, Nina Clark¹², Ernesto Cota¹³

¹National institutes of Health.

²National Institutes of Health.

³Wolters Kluwer Health.

⁴Duke University Medical Center.

⁵University of South Alabama College of Medicine.

⁶Duke University.

⁷Radboud Center for Infectious Diseases.

⁸Radboud University Medical Center, Nijmegen.

⁹Radboud University Nijmegen Medical Centre.

¹⁰National Institute of Allergy and Infectious Diseases.

¹¹Lundquist Institute for Biomedical Innovation at Harbor-UCLA.

¹²University of Illinois at Chicago.

¹³Imperial College, London.

PubMed PMC DOI PDF

Abstract

Bloodstream infection with Candida species is associated with high mortality, yet the molecular basis of vascular adhesion and invasion remains unclear. We identify the endothelial surface mucin MUC16 as a key host factor enabling fungal vascular adherence. The MUC16 SEA domain directly engages the Candida adhesin Als3p and endothelial N-cadherin to form a ternary complex that promotes endothelial…

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