دورية أكاديمية

Neutrophil-derived S100A8/A9 amplify granulopoiesis following myocardial infarction

التفاصيل البيبلوغرافية
العنوان: Neutrophil-derived S100A8/A9 amplify granulopoiesis following myocardial infarction
المؤلفون: Sreejit, Gopalkrishna, Abdel-Latif, Ahmed, Athmanathan, Baskaran, Annabathula, Rahul, Dhyani, Ashish, Noothi, Sunil K, Quaife-Ryan, Gregory A., Al-Sharea, Annas, Pernes, Gerard, Dragoljevic, Dragana, Lal, Hind, Schroder, Kate, Hanaoka, Beatriz Y., Raman, Chander, Grant, Maria B., Hudson, James E., Smyth, Susan, Porrello, Enzo R., Murphy, Andrew J., Nagareddy, Prabhakara R.
بيانات النشر: Lippincott Williams & Wilkins
سنة النشر: 2020
المجموعة: The University of Queensland: UQ eSpace
مصطلحات موضوعية: Inflammasome, Myelopoiesis, Neutrophils, S100A8/A9, interleukin 1 beta, 2705 Cardiology and Cardiovascular Medicine, 2737 Physiology (medical)
الوصف: Myocardial infarction (MI) triggers myelopoiesis resulting in heightened production of neutrophils. However, the mechanisms that sustain their production and recruitment to the injured heart are unclear. Using a mouse model of the permanent ligation of the left anterior descending (LAD) artery and flow cytometry, we first characterized the temporal and spatial effects of MI on different myeloid cell types. We next performed global transcriptome analysis of different cardiac cell types within the infarct to identify the drivers of acute inflammatory response and the underlying signaling pathways. Utilizing a combination of genetic and pharmacological strategies, we identified the sequalae of events that led to MI-induced myelopoiesis. Cardiac function was assessed by echocardiography. The association of early indices of neutrophilia with major adverse cardiovascular events (MACE) was studied in a cohort of acute MI patients. Induction of MI resulted in a rapid recruitment of neutrophils to the infarct, where they release specific alarmins, S100A8 and S100A9. These alarmins bind to the Toll Like Receptor (TLR) 4 and prime the Nod Like Receptor (NLR) family Pyrin Domain-Containing 3 (Nlrp3) inflammasome in naïve neutrophils and promote interleukin 1 (IL-1β) secretion. The released IL-1β interact with its receptor (Interleukin 1 Receptor Type 1, IL1R1) on hematopoietic stem and progenitor cells in the bone marrow (BM), and stimulate granulopoiesis in a cell-autonomous manner. Genetic or pharmacological strategies aimed at disruption of S100A8/A9 and its downstream signaling cascade suppress MI-induced granulopoiesis and improve cardiac function. Furthermore, in patients with acute coronary syndrome (ACS), higher neutrophil count on admission and post-revascularization correlates positively with major adverse cardiovascular disease (CVD) outcomes. Our study provides novel evidence for the primary role of neutrophil-derived alarmins (S100A8/A9) in dictating the nature of the ensuing inflammatory response following ...
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1524-4539
0009-7322
العلاقة: orcid:0000-0002-0012-9934; orcid:0000-0001-9261-3805; orcid:0000-0003-0832-9356; AR068450; HL122505; HL137799; HL124266; HL138488; APP1106154; APP1142938
الإتاحة: https://doi.org/10.1161/CIRCULATIONAHA.119.043833Test
https://espace.library.uq.edu.au/view/UQ:cbc800dTest
رقم الانضمام: edsbas.71EE6EC1
قاعدة البيانات: BASE