Send to

Choose Destination
J Infect Dis. 2014 Jan 1;209(1):109-19. doi: 10.1093/infdis/jit413. Epub 2013 Aug 6.

Inflammatory monocytes mediate early and organ-specific innate defense during systemic candidiasis.

Author information

Vaccine and Infectious Diseases Division.


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 postinfection. 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.


CCR2; Candida; brain; candidiasis; chemokine; fungus; graft; host defense; inflammatory; innate; kidney; monocyte; mortality; renal; sepsis; transfer; yeast

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for PubMed Central
Loading ...
Support Center