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IL-16 is constitutively present in peripheral blood monocytes and spontaneously released during apoptosis

Andreas Elssner1, Andrea I Doseff, Michelle Duncan

  • 1The Dorothy M. Davis Heart and Lung Research Institute, Ohio State University, 473 West 12th Avenue, Columbus, OH 43210, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|June 10, 2004
PubMed

Insights

Monocytes contain Interleukin-16 (IL-16), which is released during spontaneous apoptosis. This release is linked to caspase-3 activation and is inhibited by bacterial lipopolysaccharide (LPS) stimulation.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Interleukin-16 (IL-16) is constitutively expressed in various immune and non-immune cells.
  • The role of IL-16 in monocytes, particularly during apoptosis, remains largely unexplored.

Purpose of the Study:

  • To investigate the presence and release of IL-16 in human peripheral blood monocytes.
  • To determine the mechanism and regulation of IL-16 release from monocytes undergoing spontaneous apoptosis.

Main Methods:

  • Flow cytometry was used to detect intracellular IL-16 in CD14-positive monocytes.
  • Enzyme-linked immunosorbent assay (ELISA) was employed to quantify IL-16 release.
  • Caspase-3 activation and apoptosis were assessed in monocytes.
  • Monocytes were stimulated with bacterial lipopolysaccharide (LPS) to assess its effect on IL-16 release.

Main Results:

  • Freshly isolated human monocytes constitutively express IL-16 (>98%).
  • Spontaneous apoptosis in monocytes is associated with caspase-3 activation, loss of intracellular IL-16, and concurrent IL-16 release.
  • Bacterial LPS stimulation inhibited caspase-3 activation and significantly reduced IL-16 release.
  • IL-1beta and IL-8 were not released during spontaneous monocyte apoptosis, indicating specificity of IL-16 release.

Conclusions:

  • Human monocytes contain and release IL-16 during spontaneous apoptosis.
  • IL-16 release from monocytes is dependent on caspase-3 activation.
  • Bacterial LPS can inhibit IL-16 release from monocytes, suggesting a regulatory mechanism.

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