Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 209, Issue 1, Pages 109-119Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jit413
Keywords
Candida; candidiasis; fungus; sepsis; host defense; innate; kidney; renal; brain; yeast; monocyte; chemokine; CCR2; inflammatory; mortality; transfer; graft
Categories
Funding
- American Heart Association [10BGIA4340045]
- NIH [R01 093808]
- Robert A. Sinskey Foundation
- FHCRC
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI093808] Funding Source: NIH RePORTER
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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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