Area of research
Infectious Diseases · Epidemiology
Research interest
Research interests include Antifungal resistance and susceptibility, Fungal Infections and Studies, Asthma and respiratory diseases, and Antimicrobial Peptides and Activities.
Toll-like receptor 4 and CD11b expressed on microglia coordinate eradication of Candida albicans cerebral mycosis
Candidalysins Are a New Family of Cytolytic Fungal Peptide Toxins
Candida albicans: A Major Fungal Pathogen of Humans
Receptor-kinase EGFR-MAPK adaptor proteins mediate the epithelial response to Candida albicans via the cytolytic peptide toxin, candidalysin
<i>Candida albicans</i> biofilms and polymicrobial interactions
Fungal Toxins and Host Immune Responses
A variant ECE1 allele contributes to reduced pathogenicity of Candida albicans during vulvovaginal candidiasis
Candidalysin triggers epithelial cellular stresses that induce necrotic death
Role for IL-1 Family Cytokines in Fungal Infections
<i>Candida albicans</i> and candidalysin in inflammatory disorders and cancer
Candidalysin Is a Potent Trigger of Alarmin and Antimicrobial Peptide Release in Epithelial Cells
Programmed Cell Death: Central Player in Fungal Infections
Candidalysin activates innate epithelial immune responses via epidermal growth factor receptor
Candida albicans Interactions with Mucosal Surfaces during Health and Disease
Candida albicans-Induced Epithelial Damage Mediates Translocation through Intestinal Barriers
Processing of <i>Candida albicans</i> Ece1p Is Critical for Candidalysin Maturation and Fungal Virulence
IL-36 and IL-1/IL-17 Drive Immunity to Oral Candidiasis via Parallel Mechanisms
Candida–Epithelial Interactions
Candida innate immunity at the mucosa
Oral epithelial cells orchestrate innate type 17 responses to <i>Candida albicans</i> through the virulence factor candidalysin
Candidalysin Drives Epithelial Signaling, Neutrophil Recruitment, and Immunopathology at the Vaginal Mucosa
Candidalysin is a fungal peptide toxin critical for mucosal infection
IL-17 Receptor Signaling in Oral Epithelial Cells Is Critical for Protection against Oropharyngeal Candidiasis
Epithelial discrimination of commensal and pathogenic <i>Candida albicans</i>
Adaptive immune responses to<i>Candida albicans</i>infection
<i>Candida albicans-</i>epithelial interactions and pathogenicity mechanisms: scratching the surface
Candida albicans Pathogenicity and Epithelial Immunity
Protection Against Epithelial Damage During Candida albicans Infection Is Mediated by PI3K/Akt and Mammalian Target of Rapamycin Signaling