Related Experiment Video
Updated: Jun 25, 2026
Studying Microbial Communities In Vivo: A Model of Host-mediated Interaction Between Candida Albicans and Pseudomonas Aeruginosa in the Airways
Published on: January 13, 2016
Candida albicans impairs macrophage function and facilitates Pseudomonas aeruginosa pneumonia in rat
Damien Roux1, Stéphane Gaudry, Didier Dreyfuss
1INSERM U 722 and Université Paris 7-Denis Diderot, UFR de Médecine site Xavier Bichat, Paris.
Objective:
To determine whether Candida albicans airway colonization influences Pseudomonas aeruginosa pneumonia prevalence in rats and by which mechanism.
Design:
Prospective, randomized, controlled animal study.
Setting:
Research laboratory of a university.
Subjects:
Male adult Wistar rats weighing 275-300 g.
Interventions:
In vivo: P. aeruginosa pneumonia was induced by bronchial instillation of P. aeruginosa in rats previously instilled or not with live or ethanol-killed C. albicans. In vitro: Alveolar macrophages were incubated with or without live or ethanol-killed C. albicans.
Measurements And Main Results:
Quantitative cultures of lung were done. Lung tumor necrosis factor alpha, interferon gamma, and interleukin-6 levels were measured along with reactive oxygen species (ROS) production by alveolar macrophages. P. aeruginosa pneumonia prevalence was higher in rats given live but not ethanol-killed C. albicans. Instilling live C. albicans alone increased lung tumor necrosis factor-alpha and interferon-gamma but not interleukin-6, and was not associated with clinical or histologic signs of infection. These three cytokines were more abundant in lungs instilled with live C. albicans and P. aeruginosa than in those instilled with P. aeruginosa alone or with ethanol-killed C. albicans and P. aeruginosa. Alveolar macrophages incubated with live C. albicans had decreased ROS production.
Conclusions:
C. albicans impedes alveolar macrophage ROS production and is correlated with an increase of P. aeruginosa pneumonia prevalence in rats. These results highlight the previously overlooked impact of airway fungal colonization on lung bacterial infection, and indicate the need for studies on the potential for antifungal therapy to prevent the onset of ventilator-associated pneumonia caused by P. aeruginosa.
Insights
Candida albicans airway colonization increases the risk of Pseudomonas aeruginosa pneumonia in rats by reducing macrophage defenses. Antifungal therapy may help prevent bacterial pneumonia, especially in vulnerable patients.
Area of Science:
- Microbiology
- Immunology
- Pulmonology
Background:
- Fungal colonization of the airways can predispose to bacterial infections.
- The interaction between Candida albicans and Pseudomonas aeruginosa in the lung is not fully understood.
Purpose of the Study:
- To investigate if Candida albicans airway colonization affects the prevalence of Pseudomonas aeruginosa pneumonia in a rat model.
- To elucidate the underlying mechanisms of this interaction.
Main Methods:
- A prospective, randomized, controlled animal study was conducted using male Wistar rats.
- Pneumonia was induced by bronchial instillation of P. aeruginosa in rats pre-exposed to live or killed C. albicans.
- Lung cytokine levels and alveolar macrophage reactive oxygen species (ROS) production were measured.
Main Results:
- P. aeruginosa pneumonia prevalence was significantly higher in rats colonized with live C. albicans compared to controls.
- Live C. albicans colonization increased pro-inflammatory cytokines (TNF-α, IFN-γ) but decreased ROS production by macrophages.
- Ethanol-killed C. albicans did not influence P. aeruginosa pneumonia prevalence or macrophage function.
Conclusions:
- Candida albicans airway colonization impairs alveolar macrophage ROS production, increasing susceptibility to P. aeruginosa pneumonia.
- This study highlights the critical role of fungal colonization in modulating bacterial lung infections.
- Findings suggest potential benefits of antifungal therapy in preventing P. aeruginosa-associated pneumonia, particularly ventilator-associated pneumonia.
