Polymorphonuclear leukocytes (PMNs) induce protective Th1-type cytokine epithelial responses in an in vitro model of oral candidosis
| Autor: | Bernhard Hube, Gerald Hamm, Ursula Boeld, Hans C. Korting, Martin Schaller, Sylvia Oberbauer |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Keratinocytes
Chemokine Neutrophils medicine.medical_treatment Microbiology Epithelium Interferon-gamma Immune system Candidiasis Oral Candida albicans medicine Humans Interleukin 8 Cells Cultured biology Interleukin-6 Tumor Necrosis Factor-alpha Interleukin-8 Mouth Mucosa Granulocyte-Macrophage Colony-Stimulating Factor biology.organism_classification Corpus albicans Granulocyte macrophage colony-stimulating factor medicine.anatomical_structure Cytokine Immunology biology.protein Cytokines Keratinocyte Interleukin-1 medicine.drug |
| Zdroj: | Microbiology. 150:2807-2813 |
| ISSN: | 1465-2080 1350-0872 |
| DOI: | 10.1099/mic.0.27169-0 |
| Popis: | The immune response and the anticandidal activity of keratinocytes and polymorphonuclear leukocytes (PMNs) play a key role in host defence against localizedCandida albicansinfection. An established model of oral candidosis based on reconstituted human oral epithelium (RHE) was supplemented with PMNs to study the effect of these immune cells during experimental oral candidosis. Infection of RHE withC. albicansinduced a strong expression of the chemokine interleukin-8 (IL-8) and the cytokine granulocyte-macrophages colony-stimulating factor (GM-CSF), and a moderate stimulation of interleukin-1α(IL-1α), interleukin-1β(IL-1β), interleukin-6 (IL-6), interferonγ(IFN-γ) and tumour necrosis factorα(TNF-α) by keratinocytes. This immune response was associated with chemoattraction of PMNs to the site of infection, whereas uninfected RHE failed to induce cytokine expression or to attract PMNs. Growth of the pathogen and tissue damage ofC. albicans-infected RHE were significantly reduced when PMNs were applied to the apical epithelial surface or when PMNs migrated through a perforated basal polycarbonate filter of the model. Notably, protection against epithelial tissue damage was also observed when PMNs were placed on the basal side of non-perforated filters, which prevented PMN migration into the RHE. Addition of PMNs enhanced a Th1-type immune response (IFN-γ, TNF-α), down-regulated the expression of the Th2-type cytokine interleukin-10 (IL-10), and was associated with protection againstCandida-induced tissue damage. This PMN-supplemented model of oral candidosis mimics thein vivosituation, and provides a promising tool for studying the immunological interactions between keratinocytes andC. albicans, as well as the influence of PMNs onC. albicanspathogenesis. |
| Databáze: | OpenAIRE |
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