期刊
JOURNAL OF INFECTIOUS DISEASES
卷 209, 期 1, 页码 109-119出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jit413
关键词
Candida; candidiasis; fungus; sepsis; host defense; innate; kidney; renal; brain; yeast; monocyte; chemokine; CCR2; inflammatory; mortality; transfer; graft
资金
- American Heart Association [10BGIA4340045]
- NIH [R01 093808]
- Robert A. Sinskey Foundation
- FHCRC
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI093808] Funding Source: NIH RePORTER
Candida albicans is a commensal fungus that can cause systemic disease in patients with breaches in mucosal integrity, indwelling catheters, and defects in phagocyte function. Although circulating human and murine monocytes bind C. albicans and promote inflammation, it remains unclear whether C-C chemokine receptor 2 (CCR2)- and Ly6C-expressing inflammatory monocytes exert a protective or a deleterious function during systemic infection. During murine systemic candidiasis, interruption of CCR2-dependent inflammatory monocyte trafficking into infected kidneys impaired fungal clearance and decreased murine survival. Depletion of CCR2-expressing cells led to uncontrolled fungal growth in the kidneys and brain and demonstrated an essential antifungal role for inflammatory monocytes and their tissue-resident derivatives in the first 48 hours post-infection. Adoptive transfer of purified inflammatory monocytes in depleted hosts reversed the defect in fungal clearance to a substantial extent, indicating a compartmentally and temporally restricted protective function that can be transferred to enhance systemic innate antifungal immunity.
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