کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2832079 | 1163824 | 2008 | 8 صفحه PDF | دانلود رایگان |

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 108C. 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 8 × 105 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.
Journal: Molecular Immunology - Volume 45, Issue 15, September 2008, Pages 3934–3941