Sperm induce macrophage extracellular trap formation via phagocytosis-dependent mechanism

Chuncheng Lu1,2, Zhao Wu3, Hongbin Gao1,2

  • 1Department of Urology, The First Affiliated Hospital of Kunming Medical University, Kunming, China.

Insights

Sperm can trigger macrophages to release extracellular traps, a process vital for clearing abnormal sperm. This mechanism is enhanced when sperm have low motility, as seen in asthenozoospermia.

Area of Science:

  • Reproductive Immunology
  • Cellular Biology
  • Infertility Research

Background:

  • Asthenozoospermia, characterized by reduced sperm motility, is a significant cause of male infertility.
  • Macrophages in the female reproductive tract are key immune cells involved in clearing foreign entities.
  • The interaction between sperm and macrophage extracellular traps (METs) remains poorly understood.

Purpose of the Study:

  • To investigate the induction of macrophage extracellular traps by sperm.
  • To elucidate the mechanisms underlying sperm-induced MET production.
  • To explore the role of METs in the context of asthenozoospermia.

Main Methods:

  • Utilized phorbol myristate acetate (PMA)-differentiated THP-1 cells as a model for human macrophages.
  • Visualized sperm-induced METs using immunofluorescence and scanning electron microscopy.
  • Analyzed the relationship between phagocytosis and MET production by inhibiting key pathways like NADPH oxidase.

Main Results:

  • Sperm successfully triggered PMA-differentiated THP-1 macrophages to release extracellular traps.
  • Sperm-triggered MET formation was found to be dependent on macrophage phagocytosis and NADPH oxidase activity.
  • Sperm from asthenozoospermia donors induced greater MET release compared to sperm from healthy donors due to increased phagocytosis.

Conclusions:

  • Confirmed the phenomenon of sperm-induced macrophage extracellular trap formation in vitro.
  • Provided partial mechanistic insights, highlighting the roles of phagocytosis and NADPH oxidase.
  • Suggests a potential mechanism for clearing hypomotile sperm in the female reproductive tract and offers rationale for reduced fertilization probability in asthenozoospermia.

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