کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2832079 1163824 2008 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida albicans
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida albicans
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 45, Issue 15, September 2008, Pages 3934–3941
نویسندگان
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