Home > Publications Database > The effects of interleukin-6-receptor inhibition on monocytes in STEMI: a substudy of the ASSAIL-MI trial. > print

001     282292
005     20251212103343.0
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041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Huse, Camilla
|b 0
245 _ _ |a The effects of interleukin-6-receptor inhibition on monocytes in STEMI: a substudy of the ASSAIL-MI trial.
260 _ _ |a Amsterdam [u.a.]
|c 2025
|b Elsevier
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520 _ _ |a Interleukin-6 receptor (IL-6R) inhibition by tocilizumab improves myocardial salvage index (MSI) in ST-elevation myocardial infarction (STEMI). However, the mechanisms for this effect remain unclear.This pre-defined exploratory sub-study of the ASSAIL-MI trial enumerated circulating monocytes and examined their transcriptome profile in relation to the MSI and peak troponin T (TnT) in STEMI patients randomiseded to tocilizumab (n = 101) or placebo (n = 98). RNA sequencing was performed on peripheral monocytes in 14 patients. To elaborate the in vivo findings, in vitro chemotaxis and apoptosis assays were performed on THP-1 monocytes and cardiomyocyte (HL-1) cell lines, respectively.STEMI patients had increased monocyte counts at 24 h and 3-7 days after hospitalisation/PCI and this increase was attenuated by tocilizumab. Lower monocyte levels at 24 h were associated with lower TnT levels and higher MSI. Monocyte gene expression suggested that tocilizumab modulated cytokine signalling pathways related to myocardial remodelling, apoptosis, and chemotaxis, potentially through a decrease in suppressor of cytokine signalling 3 (SOCS3). In vitro, tocilizumab limited apoptosis of cardiomyocytes exposed to ischemia/reperfusion and reduced chemotaxis in monocytes exposed to IL-6.These findings suggest that IL-6R inhibition by tocilizumab during STEMI is associated with reduced monocyte counts and cardioprotective alterations in monocyte signalling potentially linked to the downregulation of SOCS3.This work was supported by the South-Eastern Norway Regional Health Authority (no. 2019067) and The Research Council of Norway (no. 282867) The ASSAIL-MI main study was supported by an independent grant from ROCHE who also provided drugs/placebo for infusion.
536 _ _ |a 354 - Disease Prevention and Healthy Aging (POF4-354)
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650 _ 7 |a Apoptosis
|2 Other
650 _ 7 |a Chemotaxis
|2 Other
650 _ 7 |a Interleukin 6
|2 Other
650 _ 7 |a Interleukin inhibition
|2 Other
650 _ 7 |a Monocytes
|2 Other
650 _ 7 |a Myocardial infarction
|2 Other
650 _ 7 |a Suppressor of cytokine signalling 3
|2 Other
650 _ 7 |a tocilizumab
|0 I031V2H011
|2 NLM Chemicals
650 _ 7 |a Receptors, Interleukin-6
|2 NLM Chemicals
650 _ 7 |a Antibodies, Monoclonal, Humanized
|2 NLM Chemicals
650 _ 7 |a Suppressor of Cytokine Signaling 3 Protein
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Monocytes: metabolism
|2 MeSH
650 _ 2 |a Monocytes: drug effects
|2 MeSH
650 _ 2 |a ST Elevation Myocardial Infarction: drug therapy
|2 MeSH
650 _ 2 |a ST Elevation Myocardial Infarction: metabolism
|2 MeSH
650 _ 2 |a ST Elevation Myocardial Infarction: blood
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Receptors, Interleukin-6: antagonists & inhibitors
|2 MeSH
650 _ 2 |a Receptors, Interleukin-6: metabolism
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Antibodies, Monoclonal, Humanized: therapeutic use
|2 MeSH
650 _ 2 |a Antibodies, Monoclonal, Humanized: pharmacology
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Apoptosis: drug effects
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Myocytes, Cardiac: metabolism
|2 MeSH
650 _ 2 |a Myocytes, Cardiac: drug effects
|2 MeSH
650 _ 2 |a Transcriptome
|2 MeSH
650 _ 2 |a Suppressor of Cytokine Signaling 3 Protein: metabolism
|2 MeSH
650 _ 2 |a Suppressor of Cytokine Signaling 3 Protein: genetics
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700 1 _ |a Murphy, Sarah Louise
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700 1 _ |a Yang, Kuan
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700 1 _ |a Balzer, Nora Reka
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700 1 _ |a Ueland, Thor
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700 1 _ |a Tøllefsen, Ingvild Maria
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700 1 _ |a Bendz, Bjørn
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700 1 _ |a Kleveland, Ola
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700 1 _ |a Andersen, Geir Øystein
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700 1 _ |a Gullestad, Lars
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700 1 _ |a Louch, William E
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700 1 _ |a Woxholt, Sindre
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700 1 _ |a Osnes, Liv
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700 1 _ |a Aukrust, Pål
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700 1 _ |a Libby, Peter
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700 1 _ |a Halvorsen, Bente
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700 1 _ |a Dahl, Tuva B
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773 _ _ |a 10.1016/j.ebiom.2025.105960
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