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Erythrocyte-derived extracellular vesicles aggravate inflammation by promoting the proinflammatory macrophage

Yuhan Gao1, Haiqiang Jin2, Hui Tan3

  • 1Department of Blood Transfusion, Peking University People's Hospital, Beijing, China.

Journal of Leukocyte Biology
|April 12, 2022
PubMed

Insights

Red blood cell extracellular vesicles (EVs) worsen sepsis outcomes by promoting inflammation. These EVs exacerbate inflammatory responses and reduce survival rates in septic mice, highlighting their role in transfusion-related complications.

Area of Science:

  • Immunology
  • Hematology
  • Cell Biology

Background:

  • Stored erythrocytes (red blood cells) are linked to increased morbidity and mortality in critical infections.
  • Red blood cell-derived extracellular vesicles (EVs) are implicated in transfusion-related immunomodulation, but mechanisms are unclear.

Purpose of the Study:

  • To investigate the effects of red blood cell-derived EVs under inflammatory conditions.
  • To explore the underlying mechanisms by which EVs influence inflammatory responses.

Main Methods:

  • In vivo evaluation of EVs in a cecal ligation and puncture (CLP)-induced sepsis model in mice.
  • In vitro assessment of EVs on lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs).
  • Analysis of inflammatory cytokine production and macrophage polarization.

Main Results:

  • EVs aggravated sepsis by increasing pro-inflammatory factors (TNF-α, IL-6, IL-1β) and reducing survival in septic mice.
  • Adoptive transfer of EV-pretreated BMDMs worsened systemic inflammation in septic mice.
  • In vitro, EVs enhanced LPS-induced pro-inflammatory cytokine production and promoted a pro-inflammatory macrophage phenotype.

Conclusions:

  • Red blood cell-derived EVs exacerbate sepsis-induced inflammation and mortality.
  • EVs promote pro-inflammatory macrophage activation and polarization.
  • EV-mediated TLR4-MyD88-NF-κB-MAPK pathway activation may underlie these effects.
Keywords:
extracellular vesicleinflammatory responsemacrophage

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