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Infection and Immunity, January 2004, p. 414-429, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.414-429.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Gene Expression in HL60 Granulocytoids and Human Polymorphonuclear Leukocytes Exposed to Candida albicans

Alaka Mullick,^1* Miria Elias,¹ Penelope Harakidas,¹ Anne Marcil,¹ Malcolm Whiteway,¹ Bing Ge,² Thomas J. Hudson,² Antoine W. Caron,¹ Lucie Bourget,¹ Serge Picard,¹ Orce Jovcevski,¹ Bernard Massie,^1,3,4 and David Y. Thomas^1,

Biotechnology Research Institute, Montréal, Québec H4P 2R2,¹ INRS-IAF, University of Québec, Laval, Québec H7N 4Z3,³ Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Montréal, Québec H3C 3J7,⁴ Montreal Genome Centre, McGill University Health Centre, Montréal, Québec H3G 1A4, Canada²

Received 3 April 2003/ Returned for modification 8 May 2003/ Accepted 1 October 2003

Candida albicans is an opportunistic human pathogen causing both superficial and disseminated diseases. It is a dimorphic fungus, switching between yeast and hyphal forms, depending on cues from its microenvironment. Hyphae play an important role in the pathogenesis of candidiasis. The host's response to Candida infection is multifaceted and includes the participation of granulocytes as key effector cells. The aim of this investigation was to study host gene expression during granulocyte-Candida interaction. Effector cells were generated by the granulocytic differentiation of HL60 cells. The resulting cell population was shown to be morphologically and functionally equivalent to granulocytes and is therefore referred to as HL60 granulocytoids for the purposes of this study. Gene expression profiles were determined 1 h after hosts were infected with C. albicans. Three Candida-granulocytoid ratios were chosen to reflect different degrees of HL60 granulocytoid inhibition of C. albicans. The data demonstrate that at the high pathogen-host ratio, C. albicans modulated the HL60 granulocytoid's response by downregulating the expression of known antimicrobial genes. In addition, looking at the expression of a large number of genes, not all of which have necessarily been implicated in candidastatic or candidacidal mechanisms, it has been possible to describe the physiological response of the HL60 granulocytoid to an infectious challenge with C. albicans. Finally, some of the observed changes in HL60 granulocytoid gene expression were investigated in freshly isolated human polymorphonuclear leukocytes infected with C. albicans. Similar changes were seen in these primary human cells, lending support to the validity of this model.

This is National Research Council publication number 46168.

Editor: T. R. Kozel

Present address: Biochemistry Department, McGill University, Montréal, Québec, Canada H3G 1Y6.

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