Effect of Interleukin-17 in the Activation of Monocyte Subsets in Patients with ST-Segment Elevation Myocardial Infarction

J Immunol Res. 2020 Jun 27;2020:5692829. doi: 10.1155/2020/5692829. eCollection 2020.

Abstract

Interleukin- (IL-) 17 is increased in acute myocardial infarction (AMI) and plays a key role in inflammatory diseases through its involvement in the activation of leukocytes. Here, we describe for the first time the effect of IL-17 in the migration and activation of monocyte subsets in patients during ST-segment elevation myocardial infarction (STEMI) and post-STEMI. We analyzed the circulating levels of IL-17 in patient plasma. A gradual increase in IL-17 was found in STEMI and post-STEMI patients. Additionally, IL-17 had a powerful effect on the recruitment of CD14++CD16+/CD14+CD16++ monocytes derived from patients post-STEMI compared with the monocytes from patients with STEMI, suggesting that IL-17 recruits monocytes with inflammatory activity post-STEMI. Furthermore, IL-17 increased the expression of TLR4 on CD14 + CD16 - and CD14++CD16+/CD14+CD16++ monocytes post-STEMI and might enhance the response to danger-associated molecular patterns post-STEMI. Moreover, IL-17 induced secretion of IL-6 from CD14++CD16- and CD14++CD16+/CD14+CD16++ monocytes both in STEMI and in post-STEMI, which indicates that IL-17 has an effect on the secretion of proinflammatory cytokines from monocytes during STEMI and post-STEMI. Overall, we demonstrate that in STEMI and post-STEMI, IL-17 is increased and induces the migration and activation of monocyte subsets, possibly contributing to the inflammatory response through TLR4 and IL-6 secretion.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Electrocardiography
  • Endothelium, Vascular / metabolism*
  • Endothelium, Vascular / pathology
  • Female
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Interleukin-17 / metabolism*
  • Interleukin-6 / metabolism
  • Lipopolysaccharide Receptors / metabolism
  • Male
  • Middle Aged
  • Monocytes / immunology*
  • Myocardial Infarction / immunology*
  • Receptors, IgG / metabolism
  • Toll-Like Receptor 4 / metabolism

Substances

  • Interleukin-17
  • Interleukin-6
  • Lipopolysaccharide Receptors
  • Receptors, IgG
  • Toll-Like Receptor 4