Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction

Sreejit, Gopalkrishna; Abdel‐Latif, Ahmed; Athmanathan, Baskaran; Annabathula, Rahul; Dhyani, A.; 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 S.; Porrello, Enzo R.; Murphy, Andrew; Nagareddy, Prabhakara R

doi:10.1161/circulationaha.119.043833

Cited by 203 publications

(218 citation statements)

References 42 publications

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“…Finally, myelopoiesis following myocardial infarction is driven by neutrophil-derived IL-1b. Neutrophils recruited to the infarcted tissue release the alarmins S100A8 and S100A9 that bind to TLR4 on naïve neutrophils and induce NLRP3 inflammasome-dependent IL-1b secretion, which subsequently drives IL-1R1-dependent granulopoiesis in the bone marrow (71). Together, IL-1 signaling is either directly or indirectly capable of inducing neutrophil production, recruitment, degranulation, and NETosis.…”

Section: Neutrophilsmentioning

confidence: 99%

Alternative Pathways of IL-1 Activation, and Its Role in Health and Disease

2020

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Cytokines activate or inhibit immune cell behavior and are thus integral to all immune responses. IL-1α and IL-1β are powerful apical cytokines that instigate multiple downstream processes to affect both innate and adaptive immunity. Multiple studies show that IL-1β is typically activated in macrophages after inflammasome sensing of infection or danger, leading to caspase-1 processing of IL-1β and its release. However, many alternative mechanisms activate IL-1α and IL-1β in atypical cell types, and IL-1 function is also important for homeostatic processes that maintain a physiological state. This review focuses on the less studied, yet arguably more interesting biology of IL-1. We detail the production by, and effects of IL-1 on specific innate and adaptive immune cells, report how IL-1 is required for barrier function at multiple sites, and discuss how perturbation of IL-1 pathways can drive disease. Thus, although IL-1 is primarily studied for driving inflammation after release from macrophages, it is clear that it has a multifaceted role that extends far beyond this, with various unconventional effects of IL-1 vital for health. However, much is still unknown, and a detailed understanding of cell-type and context-dependent actions of IL-1 is required to truly understand this enigmatic cytokine, and safely deploy therapeutics for the betterment of human health.

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Section: Neutrophilsmentioning

confidence: 99%

Alternative Pathways of IL-1 Activation, and Its Role in Health and Disease

2020

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“…chronic inflammatory disorders) can also influence the number and ratio of monocyte subsets. [212][213][214][215]…”

Section: Monocyte Origins and Egress From Bmmentioning

confidence: 99%

Origins and diversity of macrophages in health and disease

et al. 2020

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Macrophages are the first immune cells in the developing embryo and have a central role in organ development, homeostasis, immunity and repair. Over the last century, our understanding of these cells has evolved from being thought of as simple phagocytic cells to master regulators involved in governing a myriad of cellular processes. A better appreciation of macrophage biology has been matched with a clearer understanding of their diverse origins and the flexibility of their metabolic and transcriptional machinery. The understanding of the classical mononuclear phagocyte system in its original form has now been expanded to include the embryonic origin of tissue‐resident macrophages. A better knowledge of the intrinsic similarities and differences between macrophages of embryonic or monocyte origin has highlighted the importance of ontogeny in macrophage dysfunction in disease. In this review, we provide an update on origin and classification of tissue macrophages, the mechanisms of macrophage specialisation and their role in health and disease. The importance of the macrophage niche in providing trophic factors and a specialised environment for macrophage differentiation and specialisation is also discussed.

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“…However, the abundance of S100A8/A9 proteins in platelets was almost negligible in comparison with that in neutrophils after MI (Sreejit et al, 2020).…”

Section: S100a8/a9 In MImentioning

confidence: 81%

S100A8/A9 in Myocardial Infarction: A Promising Biomarker and Therapeutic Target

Cai

Xie

et al. 2020

Front. Cell Dev. Biol.

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Myocardial infarction (MI), the main cause of cardiovascular-related deaths worldwide, has long been a hot topic because of its threat to public health. S100A8/A9 has recently attracted an increasing amount of interest as a crucial alarmin that regulates the pathogenesis of cardiovascular disease after its release from myeloid cells. However, the role of S100A8/A9 in the etiology of MI is not well understood. Here, we elaborate on the critical roles and potential mechanisms of S100A8/A9 driving the pathogenesis of MI. First, cellular source of S100A8/A9 in infarcted heart is discussed. Then we highlight the effect of S100A8/A9 heterodimer in the early inflammatory period and the late reparative period of MI as well as myocardial ischemia/reperfusion (I/R) injury. Moreover, the predictive value of S100A8/A9 for the risk of recurrence of cardiovascular events is elucidated. Therefore, this review focuses on the molecular mechanisms of S100A8/A9 in MI pathogenesis to provide a promising biomarker and therapeutic target for MI.

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Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction

Cited by 203 publications

References 42 publications

Alternative Pathways of IL-1 Activation, and Its Role in Health and Disease

Alternative Pathways of IL-1 Activation, and Its Role in Health and Disease

Origins and diversity of macrophages in health and disease

S100A8/A9 in Myocardial Infarction: A Promising Biomarker and Therapeutic Target

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