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Table of Contents
Vol. 3, No. 2, 2011
Issue release date: February 2011
Section title: Research Article
Free Access
J Innate Immun 2011;3:180–199

Organ-Specific Innate Immune Responses in a Mouse Model of Invasive Candidiasis

Lionakis M.S.a · Lim J.K.a · Lee C.-C.R.b · Murphy P.M.a
aMolecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, and bLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Md., USA
email Corresponding Author

Dr. Philip M. Murphy

Molecular Signaling Section, Laboratory of Molecular Immunology

National Institutes of Health, Building 10, Room 11N113, 9000 Rockville Pike

Bethesda, MD 20892 (USA)

Tel. +1 301 496 8616, Fax +1 301 402 4369, E-Mail pmm@nih.gov

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In a fatal mouse model of invasive candidiasis (IC), fungal burden changes with variable dynamics in the kidney, brain, spleen, and liver and declines in all organs except for the kidney, which inexorably loses function. Since leukocytes are required to control Candida, we hypothesized that differential leukocyte infiltration determines organ-specific outcome of the infection. We defined leukocyte accumulation in the blood, kidney, brain, spleen, and liver after infection using fluorescent-activated cell sorting (FACS) and immunohistochemistry. Accumulation of Ly6cintCD11b+ neutrophils predominated in all organs except the brain, where CD45intCD11b+CD11c microglia were the major leukocytes detected, surrounding foci of invading Candida. Significantly more neutrophils accumulated in the spleen and liver than in the kidney during the first 24 h after infection, when neutrophil presence is critical for Candida control. Conversely, at later time points only the kidney continued to accumulate neutrophils, associated with immunopathology and organ failure. The distribution of neutrophils was completely different in each organ, with large abscesses exclusively forming in the kidney. Candida filamentation, an essential virulence factor, was seen in the kidney but not in the spleen or liver. IC induced Ly6chiCD11b+ inflammatory monocyte and NK1.1+ cell expansion in the blood and all organs tested, and MHCII+F4/80+CD11c macrophage accumulation, mainly in the spleen and liver. This study is the first detailed analysis of leukocyte subsets accumulating in different target organs during IC. The results delineate immune responses to the same pathogen that are highly idiosyncratic for each organ tested. The work provides novel insights into the balance between effective host defense and immunopathology in IC.

© 2010 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Research Article

Received: August 05, 2010
Accepted: September 10, 2010
Published online: November 09, 2010
Issue release date: February 2011

Number of Print Pages: 20
Number of Figures: 6
Number of Tables: 0

ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)

For additional information: http://www.karger.com/JIN

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