Phagocytosis of Aspergillus fumigatus conidia by murine macrophages involves recognition by the dectin-1 beta-glucan receptor and Toll-like receptor 2

被引:159
|
作者
Luther, Kathrin
Torosantucci, Antonella
Brakhage, Axel A.
Heesemann, Juergen
Ebel, Frank
机构
[1] Univ Munich, Max Von Pettenkofer Inst, Munich, Germany
[2] Ist Super Sanita, Dept Infect Parasit & Immunomediated Dis, I-00161 Rome, Italy
[3] Univ Jena, D-07745 Jena, Germany
[4] Leibnitz Inst Nat Prod Res & Infect Biol, HKI, D-07745 Jena, Germany
关键词
D O I
10.1111/j.1462-5822.2006.00796.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Aspergillus fumigatus is a fungal pathogen causing severe infections in immunocompromised patients. For clearance of inhaled conidia, an efficient response of the innate immune system is required. Macrophages represent the first line of defence and ingest and kill conidia. C-type lectins represent a family of receptors, which recognize pathogen-specific carbohydrates. One of them is beta 1-3 glucan, a major component of the fungal cell wall. Here we provide evidence that beta 1-3 glucan plays an important role for the elimination of A. fumigatus conidia. Laminarin, a soluble beta 1-3 glucan and antibodies to dectin-1, a well known beta 1-3 glucan receptor, significantly inhibited conidial phagocytosis. On resting conidia low amounts of surface accessible beta 1-3 glucan were detected, whereas high amounts were found on small spores that appear early during germination and infection as well as on resting conidia of a pksP mutant strain. Swollen conidia also display larger quantities of beta 1-3 glucan, although in an irregular spotted pattern. Resting pksP mutant conidia and swollen wild-type conidia are phagocytosed with high efficiency thereby confirming the relevance of beta 1-3 glucans for conidial phagocytosis. Additionally we found that TLR2 and the adaptor protein MyD88 are required for efficient conidial phagocytosis, suggesting a link between the TLR2-mediated recognition of A. fumigatus and the phagocytic response.
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页码:368 / 381
页数:14
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