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Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
Modulation of neutrophil function in host defense against disseminated Candida albicans infection in mice
B J Kullberg1, M G Netea, A G Vonk
1Department of Medicine, Catholic University Nijmegen and University Hospital, Nijmegen, The Netherlands.
Abstract:
Neutrophils (PMNs) constitute the main mechanism of host defense against acute invasive and disseminated candidiasis. Recent studies have demonstrated that tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF) play an important role in the recruitment of PMNs at the site of invasive Candida infection. In the absence of either TNFalpha or IL-6, the course of experimental disseminated candidiasis is more severe, due to defective PMN recruitment. Treatment of mice with recombinant G-CSF (rG-CSF) leads to a significantly reduced mortality during disseminated candidiasis. The outgrowth of Candida albicans from the organs of rG-CSF-treated mice is significantly decreased. Treatment with the combination of rG-CSF and fluconazole has an additive effect on the reduction of fungal load in the organs. In subacute or chronic disseminated Candida infection, rG-CSF is less effective, indicating that neutrophil recruitment and activation are crucial in acute, life-threatening candidiasis, whereas other host defense mechanisms control the outcome of less overwhelming invasive Candida infection.
Insights
Neutrophil recruitment is vital for combating invasive Candida infections. Granulocyte colony-stimulating factor (G-CSF) treatment reduces mortality and fungal load in acute candidiasis, especially when combined with fluconazole.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Neutrophils (PMNs) are critical for host defense against invasive candidiasis.
- Tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), and granulocyte colony-stimulating factor (G-CSF) influence PMN recruitment to Candida infection sites.
- Deficiencies in TNFalpha or IL-6 exacerbate experimental disseminated candidiasis due to impaired PMN recruitment.
Purpose of the Study:
- To investigate the role of G-CSF in experimental disseminated candidiasis.
- To evaluate the efficacy of recombinant G-CSF (rG-CSF) alone and in combination with fluconazole.
- To determine the importance of neutrophil recruitment in acute versus subacute/chronic invasive Candida infections.
Main Methods:
- Treatment of mice with rG-CSF during experimental disseminated candidiasis.
- Assessment of mortality rates and fungal load (Candida albicans outgrowth) in organs.
- Evaluation of combination therapy with rG-CSF and fluconazole.
Main Results:
- rG-CSF treatment significantly reduced mortality in disseminated candidiasis.
- rG-CSF significantly decreased Candida albicans outgrowth from organs.
- Combination therapy with rG-CSF and fluconazole showed an additive effect in reducing fungal burden.
- rG-CSF was less effective in subacute or chronic disseminated Candida infections.
Conclusions:
- Neutrophil recruitment and activation are crucial for controlling acute, life-threatening candidiasis.
- rG-CSF is a promising therapeutic agent for acute invasive candidiasis, particularly in combination with antifungals.
- Other host defense mechanisms are more important for managing less severe, chronic forms of invasive Candida infection.
