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Infection and Immunity, October 2000, p. 5628-5634, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Defective Induction of Interleukin-12 in Human Monocytes by Germ-Tube Forms of Candida albicans

Paola Chiani, Carla Bromuro, and Antonella Torosantucci*

Department of Bacteriology and Medical Mycology, Istituto Superiore di Sanità, Rome, Italy

Received 7 February 2000/Returned for modification 10 March 2000/Accepted 28 June 2000

Yeast (Y) to germ-tube (GT) transition of Candida albicans is considered a putative virulence trait. On the other hand, interleukin-12 (IL-12) is a key promoter of T-helper type 1 protective immunity against this human opportunistic pathogen. We studied IL-12 production by human monocytes cocultured in vitro with Y or GT forms of C. albicans. Following stimulation by Y cells, monocytes produced appreciable levels of IL-12, which, upon addition of gamma interferon (IFN-gamma ), compared to those achievable by lipopolysaccharide (100 ng/ml) stimulation (140 ± 65 and 185 ± 80 pg/ml, respectively [mean ± standard deviation in four independent experiments]). In contrast, IL-12 production by GT cell-stimulated monocytes was much lower or absent (<5 pg/ml) and could not be brought to the level induced by Y cells by the addition of IFN-gamma (30 ± 10 pg/ml in the four independent experiments above). Besides being observed as actual cytokine production, this lower response was also observed as specific IL-12 p40 mRNA transcript and was not associated with hyperproduction of the IL-12-competing cytokine IL-10. Phagocytosis and killing experiments in the presence of cytochalasin D showed that IL-12 production by Y cell-stimulated monocytes was phagocytosis dependent and that GT cells of C. albicans were not phagocytized by the human monocytes. Importantly, however, Y and GT cells were equally killed by the monocytes. Thus, the virulence trait attributed to the Y-GT transition of C. albicans might also be related to the lack of induction by GT cells of a protective anticandidal immunity through defective IL-12 production.

* Corresponding author. Mailing address: Department of Bacteriology and Medical Mycology, Istituto Superiore di Sanità, Viale Regina Elena, 299 00161 Rome, Italy. Phone: 39-0649902824. Fax: 39-06-49387112. E-mail: torosan{at}iss.it.

Infection and Immunity, October 2000, p. 5628-5634, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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