Journal of Andrology
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Published-Ahead-of-Print June 28, 2006, DOI:10.2164/jandrol.106.000083
Journal of Andrology, Vol. 27, No. 6, November/December 2006
Copyright © American Society of Andrology
DOI: 10.2164/jandrol.106.000083

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Spermicidal Activity of Bacterial Lipopolysaccharide Is Only Partly Due to Lipid A

HAMID HAKIMI*, IAN GEARY*, ALLAN PACEY{dagger} AND ADRIAN ELEY*

From the * Division of Genomic Medicine, The Medical School; and the {dagger} Division of Clinical Sciences, The Jessop Wing, Central Sheffield University Hospitals Trust, The University of Sheffield, Sheffield, United Kingdom.

Correspondence to: Dr Adrian Eley, Division of Genomic Medicine, The Medical School, The University of Sheffield, Sheffield, S10 2RX, United Kingdom (e-mail: a.r.eley{at}sheffield.ac.uk).


We have previously shown that co-incubation of Chlamydia trachomatis lipopolysaccharide (LPS) leads to premature sperm death by an apoptosis-like mechanism. It was always assumed that lipid A is the toxic component of LPS. Here we investigate the possible involvement of 3-deoxy-D-manno-octulosonic acid (Kdo), which is an additional component of the LPS in C. trachomatis. Highly motile preparations of sperm from normozoospermic patients were incubated for 6 hours with commercial sources of lipid A and Kdo. Conventional lipid A inhibitors, polymyxin B (PMB) and anti-CD14 monoclonal antibody (mAb) were used to test the ability of both lipid A and Kdo to induce an apoptotic-like response in mature sperm. Flow cytometry was used to determine apoptosis by the expression of annexin V. Caspase activity was also measured by fluorometry and by the use of a pan-caspase inhibitor and caspase-3 inhibitor. Both lipid A and Kdo at 50 µg/mL caused significant mortality of sperm. However, although PMB and anti-CD14 mAb were inhibitory to the activity of lipid A on sperm, no such effect was seen against Kdo. In the presence of either lipid A or Kdo, sperm death was caused by an apoptotic-like effect that was caspase mediated. We conclude that Kdo shares its spermicidal properties with lipid A and seems to kill sperm in a similar manner. These results provide an explanation for higher than expected levels of spermicidal activity of LPS that are not caused by lipid A.

     Key words: Apoptosis, human sperm, Kdo






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