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International Immunology Advance Access originally published online on November 4, 2004
International Immunology 2004 16(12):1761-1768; doi:10.1093/intimm/dxh177
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© 2004 The Japanese Society for Immunology

High dissemination and hepatotoxicity in rats infected with Candida albicans after stress exposure: potential sensitization to liver damage

Silvia Graciela Correa1, María Cecilia Rodríguez-Galán1, Beatriz Salido-Rentería1, Roxana Cano1, Hugo Cejas2 and Claudia Elena Sotomayor1

1 Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas and 2 Cátedra de Patología, Servicio de Anatomía Patológica, Hospital Misericordia, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina

Correspondence to: C. E. Sotomayor; E-mail: csotomay{at}bioclin.fcq.unc.edu.ar

The liver constitutes the first barrier in the control of hematogenous dissemination for Candida albicans of intestinal origin. The ability of this organ to limit the growth of the yeast and to mount an efficient inflammatory reaction is crucial in determining the outcome of the fungal infection. When rats infected with C. albicans are exposed to chronic varied stress, the cell recruitment is impaired at the site of the infection, the tissue reaction is highly disorganized in target organs and the infection evolution is more severe. At hepatic level, higher fungal burden is associated with hyphal form and the consistent presence of steatosis (fatty liver). Herein we aimed at characterizing the steatosis associated with C. albicans infection and to provide molecular evidence of the correlation among liver injury markers, stress products and the initiation of the inflammatory tissue reaction. After 3 days of stress and infection, we observed micro and macro steatosis in acinar zone 1 (specific lipid stain), higher lipid peroxidation and increased levels of serum alanine aminotransferase and gamma glutamil transferase. While infection triggered hepatic NO production and arginase activity, stress down-modulated both. Remarkably, defects in levels of TNF-{alpha} and NO were observed during the first step of the inflammatory response. Our results demonstrate that stress mediators down-regulate the acute inflammatory reaction in the hepatic scenario, promoting a major liver injury with particular immunopathological traits.

Keywords: arginase, fungal infection, iNOS, lipid peroxidation, rats, steatosis, TNF-{alpha}

Transmitting editor: A. Falus


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[Abstract] [Full Text] [PDF]


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