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The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis

Shuo Geng1, Keqiang Chen1, Ruoxi Yuan1

  • 1Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.

Nature Communications
|November 9, 2016
PubMed

Insights

Subclinical endotoxemia programs monocytes into a non-resolving inflammatory state, worsening atherosclerosis. This occurs via elevated miR-24 and reduced IRAK-M, disrupting monocyte homeostasis and promoting chronic inflammation.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Sustained low-grade inflammation, driven by non-resolving inflammatory monocytes, is implicated in atherosclerosis pathogenesis.
  • The precise molecular mechanisms sustaining these monocytes in atherosclerosis remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms driving the sustainment of non-resolving inflammatory monocytes in atherosclerosis.
  • To investigate the role of subclinical endotoxemia in programming monocyte behavior and disease progression.

Main Methods:

  • Murine models of atherosclerosis were utilized to study monocyte programming under subclinical endotoxemia.
  • Molecular analyses focused on microRNA (miR-24), negative-feedback regulators (IRAK-M), and key cellular markers (Ly6C, CCR5, MCP-1, SR-B1).

Main Results:

  • Subclinical endotoxemia aggravated murine atherosclerosis by inducing a non-resolving inflammatory monocyte phenotype (elevated Ly6C, CCR5, MCP-1; reduced SR-B1).
  • Monocyte homeostasis disruption was linked to increased miR-24 and decreased IRAK-M.
  • miR-24 was found to reduce Smad4 (for IRAK-M expression) and SR-B1.
  • IRAK-M deficiency exacerbated these effects, leading to elevated miR-24 and worsened atherosclerosis.

Conclusions:

  • An integrated feedback circuit in monocytes involving miR-24 and IRAK-M was identified.
  • Disruption of this circuit promotes non-resolving inflammation, contributing to atherosclerosis development.

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