Journal of Immunology Research (Jan 2020)

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

  • Montserrat Guadalupe Garza-Reyes,
  • Mónica Daniela Mora-Ruíz,
  • Luis Chávez-Sánchez,
  • Alejandra Madrid-Miller,
  • Alberto Jose Cabrera-Quintero,
  • José Luis Maravillas-Montero,
  • Alejandro Zentella-Dehesa,
  • Luis Moreno-Ruíz,
  • Selene Pastor-Salgado,
  • Erick Ramírez-Arias,
  • Nataly Pérez-Velázquez,
  • Adriana Karina Chávez-Rueda,
  • Francisco Blanco-Favela,
  • Wendy Guadalupe Vazquez-Gonzalez,
  • Alicia Contreras-Rodríguez

DOI
https://doi.org/10.1155/2020/5692829
Journal volume & issue
Vol. 2020

Abstract

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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.