Oral Candidiasis and Host Immune Interactions

Oral candidiasis, commonly known as thrush, arises when the normally commensal fungus Candida albicans breaches mucosal defences and causes inflammation and tissue damage. In healthy individuals, a balanced oral microbiome and innate immune barriers—including salivary antimicrobial peptides, mucosal epithelial integrity and resident phagocytes—maintain C. albicans in a benign commensal state. Perturbations such as immunosuppression, antibiotic use or denture wear can shift this equilibrium, enabling adhesion to epithelial surfaces, morphogenetic switching to invasive hyphae and formation of resilient biofilms. Pattern recognition receptors on epithelial cells and innate immune cells detect fungal cell-wall components, triggering antifungal effector responses. Neutrophils and macrophages engage in phagocytosis and release reactive oxygen species, while specialised T helper 17 lymphocytes coordinate mucosal clearance and reinforce barrier function. In some instances, excessive host-driven inflammation contributes to tissue damage, a phenomenon encapsulated in the damage response framework. The interplay between fungal virulence factors—such as secreted aspartyl proteases and adhesins—and host immune mediators determines whether colonisation remains asymptomatic or progresses to overt disease. Contemporary research seeks to unravel the molecular dialogue at the epithelial–fungal interface, the immune pathways that underpin tolerance and resistance, and strategies to prevent the transition from commensal carriage to pathogenic infection.

Research from Nature Portfolio

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Oral Candidiasis and Host Immune Interactions publication trend

The graph below shows the total number of articles in oral candidiasis and host immune interactions across all publications each year (not limited to Nature Index journals).

Technical terms

Candida albicans: A polymorphic fungal species that can exist as a harmless commensal or an invasive pathogen in the oral cavity.

Biofilm: A structured community of microbial cells encased in an extracellular matrix, adherent to surfaces and resistant to host defences and antifungal agents.

Th17 cell: A subset of CD4+ T lymphocytes that produces interleukin-17 to enhance mucosal immunity against fungal pathogens.

Damage Response Framework: A conceptual model describing how disease outcomes depend on the interplay between microbial virulence and host immune response.

Innate immunity: The first line of defence comprising physical barriers, phagocytic cells, pattern recognition receptors and soluble antimicrobial factors.

References

1. Interactions of Candida albicans with host epithelial surfaces. Journal of Oral Microbiology (2013).
2. Candida-Associated Denture Stomatitis and Murine Models: What Is the Importance and Scientific Evidence?. Journal of Fungi (2020).
3. Multi-Omics Profiling of Candida albicans Grown on Solid Versus Liquid Media. Microorganisms (2023).
4. Oral Candidiasis: A Disease of Opportunity. Journal of Fungi (2020).
5. Applying the Host-Microbe Damage Response Framework to Candida Pathogenesis: Current and Prospective Strategies to Reduce Damage. Journal of Fungi (2020).