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Infection and Immunity, November 2009, p. 4990-4997, Vol. 77, No. 11
0019-9567/09/$08.00+0 doi:10.1128/IAI.00586-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Obstetrics and Gynecology, University of Wuerzburg, Josef-Schneider Str. 4, D-97080 Wuerzburg, Germany,1 Leibniz Institute for Natural Product Research and Infection Biology-Hans Knoell Institute, Junior Research Group Fundamental Molecular Biology of Pathogenic Fungi, Beutenbergstr. 11a, D-07745 Jena, Germany2
Received 26 May 2009/ Returned for modification 2 July 2009/ Accepted 7 August 2009
Infertility in men and women is frequently associated with genital contamination by various commensal or uropathogenic microbes. Since many microorganisms are known to release quorum-sensing signals in substantial amounts, we raised the question whether such molecules can directly affect human spermatozoa. Here we show that farnesol and 3-oxododecanoyl-L-homoserine lactone, employed by the opportunistic pathogenic yeast Candida albicans and the gram-negative bacterium Pseudomonas aeruginosa, respectively, induce multiple damage in spermatozoa. A reduction in the motility of spermatozoa coincided in a dose-dependent manner with apoptosis and necrosis at concentrations which were nondeleterious for dendritic cell-like immune cells. Moreover, sublethal doses of both signaling molecules induced premature loss of the acrosome, a cap-like structure of the sperm head which is essential for fertilization. Addressing their mechanism of action, we found that the bacterial molecule, but not the fungal molecule, actively induced the acrosome reaction via a calcium-dependent mechanism. This work uncovers a new facet in the interaction of microorganisms with human gametes and suggests a putative link between microbial communication systems and host infertility.
Published ahead of print on 17 August 2009.
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