Differential Cytokine Production and Toll-Like Receptor Signaling Pathways by Candida albicans Blastoconidia and Hyphae
| Autor: | Bart Jan Kullberg, Ineke Verschueren, Chantal A. A. van der Graaf, Mihai G. Netea, Jos W. M. van der Meer |
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| Rok vydání: | 2005 |
| Předmět: |
Time Factors
Hypha medicine.medical_treatment Immunology Phenotypic switching Hyphae Biology Microbiology Blastoconidium Proinflammatory cytokine Invasive mycoses and compromised host [N4i 2] Mice Candida albicans Effective Primary Care and Public Health [EBP 3] medicine Animals Humans Mice Knockout Toll-like receptor fungi Toll-Like Receptors Candidiasis Spores Fungal biology.organism_classification Toll-Like Receptor 2 Corpus albicans Mice Inbred C57BL Toll-Like Receptor 4 Pathogenesis and modulation of inflammation [N4i 1] Infectious Diseases Cytokine Gene Expression Regulation Leukocytes Mononuclear Cytokines Parasitology Microbial pathogenesis and host defense [UMCN 4.1] Fungal and Parasitic Infections Infection and autoimmunity [NCMLS 1] Spleen Signal Transduction |
| Zdroj: | Infection and Immunity, 73, 11, pp. 7458-64 Infection and Immunity, 73, 7458-64 |
| ISSN: | 1098-5522 0019-9567 |
| DOI: | 10.1128/iai.73.11.7458-7464.2005 |
| Popis: | Toll-like receptors (TLR) are crucial for an efficient antifungal defense. We investigated the differential recognition of blastoconidia and hyphae of Candida albicans by TLRs. In contrast to Candida blastoconidia, which stimulated large amounts of gamma interferon (IFN-γ), the tissue-invasive Candida hyphae did not stimulate any IFN-γ by human peripheral blood mononuclear cells (PBMC) or murine splenic lymphocytes. After stimulation with blastoconidia, the production of IFN-γ was TLR4 dependent, as shown by the significantly decreased IFN-γ production in anti-TLR4-treated PBMC and in splenic lymphocytes from TLR4-defective ScCr mice. In addition, peritoneal macrophages from ScCr mice produced less tumor necrosis factor α (TNF-α) than macrophages of control mice did when stimulated with Candida blastoconidia, but not with hyphae, indicating that TLR4-mediated signals are lost during hyphal germination. In contrast, macrophages from TLR2 knockout mice had a decreased production of TNF-α in response to both Candida blastoconidia and hyphae. Candida hyphae stimulated production of interleukin-10 through TLR2-dependent mechanisms. In conclusion, TLR4 mediates proinflammatory cytokine induction after Candida stimulation, whereas Candida recognition by TLR2 leads mainly to anti-inflammatory cytokine release. TLR4-mediated proinflammatory signals are lost during germination of Candida blastoconidia into hyphae. Phenotypic switching during germination may be an important escape mechanism of C. albicans , resulting in counteracting host defense. |
| Databáze: | OpenAIRE |
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