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• W4229451272 abstract "HomeCirculationVol. 145, No. 19Letter by Ren and Yang Regarding Article, “Retention of the NLRP3 Inflammasome–Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction–Induced Granulopoiesis” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Ren and Yang Regarding Article, “Retention of the NLRP3 Inflammasome–Primed Neutrophils in the Bone Marrow Is Essential for Myocardial Infarction–Induced Granulopoiesis” Chuanli Ren, MD and Zhangjun Yang, PhD Chuanli RenChuanli Ren https://orcid.org/0000-0002-8386-3586 Department of Laboratory Medicine, Clinical Medical College of Yangzhou University, China (C.R.). Search for more papers by this author and Zhangjun YangZhangjun Yang Department of Chemistry, Yangzhou University, China (Z.Y.). Search for more papers by this author Originally published9 May 2022https://doi.org/10.1161/CIRCULATIONAHA.122.059645Circulation. 2022;145:e1034To the Editor:We read with interest the article by Sreejit et al,1 who found that elevated serum S100A8/A9 levels are necessary for homing and retention of the reverse-migrating neutrophils and that S100A8/A9 may fulfill its proinflammatory effect through priming the NLRP3 (nod-like receptor family pyrin domain–containing 3 inflammasome) during acute myocardial infarction. In general, S100A8/A9 is viewed as inflammatory,1 but more and more studies have revealed that it is used in both anti-inflammatory and immune regulatory roles.2 Anti-inflammatory effects of S100A proteins might be mediated by oxidation and nitrosylation of the S100A proteins, arachidonic acid binding, or other mechanisms.3 We wonder how S100A8/A9 can balance its dual proinflammatory and anti-inflammatory roles during the S100A8/A9-NLRP3-IL-1β (interleukin-1β) signaling axis in injury-exposed neutrophils. Why and how does S100A8/A9 mediate proinflammatory and anti-inflammatory effects in different types of blood-derived cells in bone marrow such as neutrophils, lymphocytes, and macrophages? It appears to have been ignored in the discussion part of the authors’ work. Overexpression of S100A8 and S00A9 in macrophages induced enhanced extracellular reactive oxygen species production, whereas it led to elevated mRNA expression of anti-inflammatory IL-10 (interleukin-10).4 Recent studies revealed insights into the biological functions of the S100A8 and S100A9 during orchestration of an inflammatory response at mucosal surfaces other than myocardial endothelial cell across organ systems. Furthermore, S100A8/A9 enhances the therapeutic paracrine effects of human amniotic mesenchymal stem cells in aspects of anti-inflammation, antifibrosis, and cardiac function preservation after myocardial infarction.5It implies that intravenous administration of the conditioned medium of S100A8/A9-pretreated human amniotic mesenchymal stem cells improved left ventricular function and decreased myocardial fibrosis after ischemia/reperfusion injury.5 After myocardial infarction, neutrophils rapidly infiltrate the infarcted heart and release various proteins, including S100A8/A9, which, in turn, initiate the NLRP3 inflammasome. Because of the dual roles of S100A8/A9 in different cells and multiple functions in different cells, it seems prudent to investigate the ability of S100A8/A9 and the NLRP3 inflammasome to specifically improve cardiovascular disease outcomes. On the basis of the seemingly paradoxical multiple functions of S100A8/A9, further studies on the proinflammatory and anti-inflammatory effects of S100A8/A9 complex in specific microenvironmental manners will ultimately inhibit granulocyte production and improve cardiac function, which may provide more valuable targets to the human cardiac treatment of vascular disease in the future.Article InformationSources of FundingThis study was supported by the National Natural Science Foundation of China (82172345).Disclosures None.FootnotesCirculation is available at www.ahajournals.org/journal/circReferences1. Sreejit G, Nooti SK, Jaggers RM, Athmanathan B, Ho Park K, Al-Sharea A, Johnson J, Dahdah A, Lee MKS, Ma J, et al.. Retention of the NLRP3 inflammasome–primed neutrophils in the bone marrow is essential for myocardial infarction–induced granulopoiesis.Circulation. 2022; 145:31–44. doi: 10.1161/CIRCULATIONAHA.121.056019LinkGoogle Scholar2. Averill MM, Kerkhoff C, Bornfeldt KE. S100A8 and S100A9 in cardiovascular biology and disease.Arterioscler Thromb Vasc Biol. 2012; 32:223–229. doi: 10.1161/ATVBAHA.111.236927LinkGoogle Scholar3. Kerkhoff C, Klempt M, Kaever V, Sorg C. The two calcium-binding proteins, S100A8 and S100A9, are involved in the metabolism of arachidonic acid in human neutrophils.J Biol Chem. 1999; 274:32672–32679. doi: 10.1074/jbc.274.46.32672CrossrefMedlineGoogle Scholar4. Jukic A, Bakiri L, Wagner EF, Tilg H, Adolph TE. Calprotectin: from biomarker to biological function.Gut. 2021; 70:1978–1988. doi: 10.1136/gutjnl-2021-324855CrossrefMedlineGoogle Scholar5. Chen TJ, Yeh YT, Peng FS, Li AH, Wu SC. S100A8/A9 enhances immunomodulatory and tissue-repairing properties of human amniotic mesenchymal stem cells in myocardial ischemia-reperfusion injury.Int J Mol Sci. 2021; 22:11175. doi: 10.3390/ijms222011175CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails May 10, 2022Vol 145, Issue 19 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.122.059645PMID: 35533215 Originally publishedMay 9, 2022 PDF download Advertisement SubjectsMyocardial Infarction" @default.
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