Interleukin-6 inhibition in ST-elevation myocardial infarction: Immune cell profile in the randomised ASSAIL-MI trial

Huse, Camilla; Anstensrud, Anne Kristine; Michelsen, Annika; Ueland, Thor; Broch, Kaspar; Woxholt, Sindre; Yang, Kuan; Sharma, Kapil; Tøllefsen, Ingvild Maria; Bendz, Bjørn; Amundsen, Brage H.; Damås, Jan Kristian; Berg, Erlend Sturle; Bjørkelund, Elisabeth; Quiles‐Jiménez, Ana; Bjerkeli, Vigdis; Bendz, Christina; Kleveland, Ola; Stensæth, Knut Haakon; Opdahl, Anders; Kløw, Nils‐Einar; Andersen, Geir Øystein; Wiseth, Rune; Halvorsen, Bente; Gullestad, Lars; Seljeflot, Ingebjørg; Aukrust, Pål; Osnes, Liv; Dahl, Tuva B.

doi:10.1016/j.ebiom.2022.104013

Cited by 29 publications

(25 citation statements)

References 43 publications

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“…The laboratory follows standard operation procedure and also has ISO (International Standard Organization) certification. Further sub-classification of T cells was performed on a Gallios Flow cytometer (Beckman Coulter, San Diego, CA, USA) as previously described ( 9 ). Reference values (5–95 percentile) for absolute numbers of T and NK-cells, and T-subpopulations were established on samples from healthy blood donors ( n = 65).…”

Section: Methodsmentioning

confidence: 99%

Markers of extracellular matrix remodeling and systemic inflammation in patients with heritable thoracic aortic diseases

Seim

Holt

Ratajska

et al. 2022

Front. Cardiovasc. Med.

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BackgroundIn approximately 20% of patients with thoracic aortic aneurysms or dissections a heritable thoracic aortic disease (HTAD) is suspected. Several monogenic connective tissue diseases imply high risk of aortic disease, including both non-syndromic and syndromic forms. There are some studies assessing inflammation and extracellular matrix remodeling in patients with non-hereditary aortic disease, but such studies in patients with hereditary diseases are scarce.AimsTo quantify markers of extracellular matrix (ECM) and inflammation in patients with vascular connective tissue diseases versus healthy controls.MethodsPatients with Loeys-Dietz syndrome (LDS, n = 12), Marfan syndrome (MFS, n = 11), and familial thoracic aortic aneurysm 6 (FTAA6, n = 9), i.e., actin alpha 2 (ACTA2) pathogenic variants, were recruited. Exome or genome sequencing was performed for genetic diagnosis. Several markers of inflammation and ECM remodeling were measured in plasma by enzyme immunoassays. Flow cytometry of T-cell subpopulations was performed on a subgroup of patients. For comparison, blood samples were drawn from 14 healthy controls.Results(i) All groups of HTAD patients had increased levels matrix metalloproteinase-9 (MMP-9) as compared with healthy controls, also in adjusted analyses, reflecting altered ECM remodeling. (ii) LDS patients had increased levels of pentraxin 3 (PTX3), reflecting systemic inflammation. (iii) LDS patients have increased levels of soluble CD25, a marker of T-cell activation.ConclusionOur data suggest that upregulated MMP-9, a matrix degrading enzyme, is a common feature of several subgroups of HTAD. In addition, LDS patients have increased levels of PTX3 reflecting systemic and in particular vascular inflammation.

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Section: Methodsmentioning

confidence: 99%

Markers of extracellular matrix remodeling and systemic inflammation in patients with heritable thoracic aortic diseases

Seim

Holt

Ratajska

et al. 2022

Front. Cardiovasc. Med.

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“…Кардиоваскулярная безопасность лечения ингибиторами ИЛ-6 была подтверждена в исследованиях ряда авторов [92][93][94]. Более того, имеются данные, свидетельствующие о важной роли ИЛ-6 в патогенезе кардиоваскулярной патологии [95][96][97] и потенциальных положительных сосудистых эффектах ТЦЗ у пациентов с инфарктом миокарда (ASSAIL-MI) [98] и новых мАТ к ИЛ-6 зилтивекимаба (ziltivekimab) в общей популяции пациентов с атеросклеротическим поражением сосудов (RESCUE) [99].…”

Section: таблица 6 сравнительная эффективность терапии ингибиторами и...unclassified

The prospects of interleukin-6 inhibition in rheumatoid arthritis: Olokizumab (novel monoclonal antibodies to IL-6)

Насонов

Feist

2022

Naučno-praktičeskaâ revmatologiâ

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Rheumatoid arthritis (RA) is a chronic immune-mediated rheumatic diseases (IMRDs) manifested with progressive destruction of joints, systemic inflammation of visceral organs and a wide range of co-morbidities associated with chronic inflammation. Among the cytokines involved in the pathogenesis of RA and certain other IMRDs, the role of interleukin (IL) 6 is of special interest. The introduction of mAbs tocilizumab (TCZ) and later sarilumab (SAR), both blocking the receptor of this cytokine, into clinical practice was an important achievement in the treatment of IIRDs at the beginning of the 21st century. As a novel approach in the treatment of RA, the humanized mAb against IL-6 olokizumab (OKZ) is in development by the Russian company R-PHARM under the license agreement with UCB Pharma. The review examines new data on efficacy and safety of OKZ in RA and the prospects of its use in rheumatology

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“…Scientists have to comprehend these immunodynamics to identify key regulators of the inflammatory process to beneficially modulate resolution of cardiac injury. Emerging therapeutic strategies aim to inhibit innate immunity targeting cytokines such IL-1β or IL-6 in CVDs [ 161 , 193 , 194 ]. In that light, the CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study) trial demonstrated that targeting IL-1β significantly lowers major cardiovascular events in 10,061 patients with previous myocardial infarction and elevated high-sensitivity C-reactive protein levels (hsCRP) [ 193 ].…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction

Moggio

Schunkert

Kessler

et al. 2022

IJMS

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Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the “leukocyte supply chain” and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI.

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Interleukin-6 inhibition in ST-elevation myocardial infarction: Immune cell profile in the randomised ASSAIL-MI trial

Cited by 29 publications

References 43 publications

Markers of extracellular matrix remodeling and systemic inflammation in patients with heritable thoracic aortic diseases

Markers of extracellular matrix remodeling and systemic inflammation in patients with heritable thoracic aortic diseases

The prospects of interleukin-6 inhibition in rheumatoid arthritis: Olokizumab (novel monoclonal antibodies to IL-6)

Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction

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