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

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.

Cellular and immunometabolic mechanisms of inflammation in depression: Preliminary findings from single cell RNA sequencing and a tribute to Bruce McEwen

“…2 B). Genes upregulated in these CD14 + monocytes, which were unique to MD with high CRP, were significantly enriched for a number of pathways related to inflammation (Phagosome, Complement system), immune cell migration (Cell adhesion molecules, IL-17 signaling pathway ( Garza-Reyes et al, 2020 )), and immunometabolic shifts thought to play a role in myeloid-driven inflammation (HIF-1 signaling, aerobic glycolysis)(all p < 0.05 and q < 0.1; Fig. 2 C, Figs.…”

The abnormal level and prognostic potency of multiple inflammatory cytokines in PCI‐treated STEMI patients

“…Inflammation is non‐negligible in STEMI etiology, which is considered an essential process that participates in the initiation and progression of atherosclerotic plaque 9–11 . Consequently, some studies notice that the increased level of inflammatory cytokines possesses a certain value in predicting the MACE risk of STEMI patients, including interleukin (IL)‐1, IL‐6, IL‐17, IL‐37, etc 12–15 . For instance, one study suggests that the high level of IL‐6 is correlated with elevated MACE risk in STEMI patients who receive primary PCI treatment 13 .…”

Single‐cell RNA Sequencing Identified Novel Nr4a1+ Ear2+ Anti‐Inflammatory Macrophage Phenotype under Myeloid‐TLR4 Dependent Regulation in Anti‐Glomerular Basement Membrane (GBM) Crescentic Glomerulonephritis (cGN)

“…Several studies have reported that activation of IL‐17 signaling can promote macrophage recruitment, [ 17 ] polarize macrophages toward a proinflammatory transcriptome, [ 18 ] or even enhance the expression of TLR4 in macrophages. [ 19 ] By using scRNA‐seq, our study firstly demonstrated the activation of IL‐17 signaling in TLR4‐dependent proinflammatory macrophage subsets at early stage of experimental anti‐GBM cGN, indicating the IL‐17 mediated downstream cascade may be another potential mechanism in anti‐GBM cGN. Compared to Cluster 0, Cluster 1 monocytes uniquely expressed neutrophil‐like gene signatures, such as S100a8, S100a9 and Lrg1 , while lacking of Ly6g expression (Figure 2C and Figure S3 , Supporting Information), suggesting their potential identity as GMPs‐derived neutrophil‐like monocytes.…”