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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

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CD16+ monocytes produce IL-6, CCL2, and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing

Petronela Ancuta1, Jianbin Wang, Dana Gabuzda

  • 1Department of Cancer Immunology, and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

Journal of Leukocyte Biology
|October 24, 2006
PubMed

Insights

CD16+ monocytes, expanded in inflammation, produce IL-6, CCL2, and MMP-9 when interacting with CX3CL1-expressing cells. This suggests a mechanism for inflammatory cell recruitment and tissue injury.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • CD16+ monocytes are elevated in inflammatory diseases like sepsis, HIV-1, and cancer.
  • CD16+ monocytes express CX3CR1, mediating adhesion to CX3CL1 on endothelial cells (EC).
  • CD16- monocyte attachment to activated EC is CX3CL1-independent.

Purpose of the Study:

  • To investigate the cytokine production of CD16+ and CD16- monocytes upon interaction with CX3CL1-expressing human umbilical vein endothelial cells (HUVEC).

Main Methods:

  • Coculture of CD16+ and CD16- monocytes with activated or nonactivated HUVEC expressing CX3CL1.
  • Measurement of cytokine (IL-6, CCL2) and matrix metalloproteinase (MMP-9) production.
  • Assessment of neuronal cell death induced by monocyte-EC coculture supernatants.

Main Results:

  • CD16+ monocytes, but not CD16- monocytes, produced significant levels of IL-6, CCL2, and MMP-9 when cocultured with activated HUVEC or CX3CL1-expressing HUVEC.
  • Supernatants from these cocultures induced neuronal death in vitro.
  • CX3CL1 engagement of CX3CR1 on CD16+ monocytes likely stimulates this cytokine and MMP production.

Conclusions:

  • Expansion and accumulation of CD16+ monocytes on CX3CL1-expressing EC contribute to inflammatory processes.
  • This interaction promotes monocyte and T cell recruitment via CCL2.
  • IL-6 may drive cell activation/differentiation, while MMP-9 mediates vascular and tissue damage.

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