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Updated: May 18, 2026

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
Deficient Candida-specific T-helper 17 response during sepsis
Frank L van de Veerdonk1, Maria Mouktaroudi, Bart P Ramakers
1Department of Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands. f.veerdonk@aig.umcn.nl
T-helper 17 (Th17) responses are reduced in patients with sepsis and endotoxemia. This deficiency in Th17 immunity increases the risk of developing invasive Candida infections in critically ill patients.
Area of Science:
- Immunology
- Infectious Diseases
- Critical Care Medicine
Background:
- Patients in intensive care units (ICUs) with sepsis are susceptible to Candida infections.
- T-helper 17 (Th17) cells play a crucial role in antifungal immunity.
Purpose of the Study:
- To investigate the impact of endotoxemia and sepsis on Candida-induced Th17 responses.
- To determine if impaired Th17 responses contribute to Candida infection susceptibility in sepsis.
Main Methods:
- Experimental human endotoxemia model.
- Analysis of Th17 responses in peripheral blood mononuclear cells (PBMCs) stimulated with Candida albicans.
- Comparison of Th17 responses between healthy controls and patients with gram-negative sepsis.
Main Results:
- Th17 response was significantly lower during experimental endotoxemia compared to baseline.
- Patients with gram-negative sepsis exhibited a significantly reduced Th17 response compared to healthy individuals.
- Candida albicans stimulation revealed impaired Th17 cell activity in sepsis.
Conclusions:
- Endotoxin-related systemic inflammation, as seen in sepsis, leads to a deficient Th17 immune response.
- Impaired Th17 immunity is a potential risk factor for the development of Candida infections in sepsis patients.
- Restoring Th17 function may be a therapeutic target to prevent invasive fungal infections in sepsis.
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