Journal of Andrology
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Published-Ahead-of-Print June 28, 2006, 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 , and Adrian Eley *

* To whom correspondence should be addressed. 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 is 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 in addition to lipid A makes up the LPS in C. trachomatis. Highly motile preparations of sperm from normozoospermic patients were incubated for 6h with commercial sources of lipid A and Kdo. Conventional lipid A inhibitors, polymyxin B (PMB), and anti-CD14 monoclonal antibody (MAb) were tested on 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 fluorimetry 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 which 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 which are not caused by lipid A.


Key words: Fertility • Infertility • Reproductive Tract • Semen • Sperm • Apoptosis • Human sperm • Kdo






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