| http://purl.uniprot.org/citations/18672286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18672286 | http://www.w3.org/2000/01/rdf-schema#comment | "Candida albicans is the major cause of systemic fungal infections in immunocompromised patients. We investigated the susceptibility of mice deficient in complement factor B and C2 (Bf/C2-/-), C1q (C1qa-/-), and mannan-binding lectin (MBL)-A (MBL-A) and MBL-C (MBL-A/C-/-) to systemic infection with C. albicans. Animals were infected i.p. with 10(8)C. albicans blastoconidia and monitored for mortality. Bf/C2-/-mice showed high mortality (over 90%) within the study period of 3 weeks. In contrast, mortality in C1qa-/- mice was below 15% whereas that of MBL-A/C-/-mice was 40% (P<0.001). Intravenous infection of mice with 8x10(5) blastoconidia resulted in the same trend with Bf/C2-/-mice being highly susceptible compared to the other strains. Histology of kidney sections of infected Bf/C2-/-mice showed widespread mycelia confirming the high CFU counts from cultured tissue homogenates. In C1qa-/-, MBL-A/C-/- and wild type C57BL/6 mice hyphal growth was limited. However, massive inflammatory infiltration was apparent, which was not seen in Bf/C2-/-mice. The ability of the mouse sera to opsonize C. albicans was determined by quantification of phagocytosis of C. albicans by peritoneal phagocytes. Whilst phagocytosis mediated by Bf/C2-/-mouse serum was low (10.6%), more phagocytosis could be seen in MBL-A/C-/-(19.9%), C1qa-/-mice (23.9%) and wild type mice (29%). Deficiency of classical pathway activation has only a low impact whereas the lectin pathway contributes to the host defence against candidosis. The more pronounced lack of complement activation in Bf/C2-/-mice leads to uncontrolled infection due to an opsonophagocytic defect."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.molimm.2008.06.021"xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/author | "Petry F."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/author | "Held K."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/author | "Loos M."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/author | "Thiel S."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/name | "Mol Immunol"xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/pages | "3934-3941"xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/title | "Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida albicans."xsd:string |
| http://purl.uniprot.org/citations/18672286 | http://purl.uniprot.org/core/volume | "45"xsd:string |
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