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Toll-like receptors (TLR) 2 and 4 on human sperm recognize bacterial endotoxins and mediate apoptosis

Youko Fujita1, Toshihiro Mihara, Tetsuji Okazaki

  • 1Laboratory of Reproductive Endocrinology, Department of Applied Animal Science, Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Hiroshima 739-8528, Japan.

Human Reproduction (Oxford, England)
|July 22, 2011
PubMed
Abstract

Insights

Sperm can detect bacterial endotoxins via Toll-like receptors (TLRs). This recognition impairs sperm motility, increases apoptosis, and reduces fertilization potential, contributing to male infertility.

Area of Science:

  • Reproductive Biology
  • Immunology
  • Microbiology

Background:

  • Bacterial genital tract infections are a major cause of male infertility.
  • Leukocytospermia (white blood cells in semen) is linked to poor semen quality.
  • Leukocytes activate Toll-like receptor (TLR) pathways and secrete cytokines, impacting sperm motility.

Purpose of the Study:

  • To investigate the direct effects of bacterial endotoxins on sperm function.
  • To determine if sperm express TLRs and respond to bacterial components.
  • To elucidate the role of TLRs in endotoxin-induced sperm dysfunction.

Main Methods:

  • Detection of bacterial endotoxins (LPS, peptidoglycan) in human semen.
  • In vitro and in vivo assessment of sperm motility, apoptosis, and fertilization in response to endotoxins.
  • Analysis of Toll-like receptor (TLR2 and TLR4) expression in sperm.
  • Experiments using Tlr2/4(-/-) double-mutant mice to assess the role of TLRs.

Main Results:

  • Bacterial endotoxins (LPS, peptidoglycan) were found in human semen.
  • Endotoxins directly reduced sperm motility and increased apoptosis in human and mouse sperm.
  • Sperm express TLR2 and TLR4, which mediate the negative effects of endotoxins.
  • The detrimental effects of endotoxins on sperm were abolished in Tlr2/4(-/-) mice.

Conclusions:

  • Sperm possess membrane-bound TLRs capable of recognizing bacterial endotoxins.
  • Activation of TLR-dependent pathways by endotoxins leads to reduced sperm motility and increased apoptosis.
  • This TLR-mediated response significantly impairs sperm fertilization potential, contributing to infertility.

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