Redox and Src family kinase signaling control leukocyte wound attraction and neutrophil reverse migration

Tauzin, Sébastien; Starnes, Taylor W.; Barros-Becker, Francisco; Lam, Pui-ying; Huttenlocher, Anna

doi:10.1083/jcb.201408090

Cited by 116 publications

(145 citation statements)

References 32 publications

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“…Moreover, macrophage-depletion shows an increased number of neutrophils under inflammatory conditions, pointing to uncontrolled neutrophil recruitment. However, the macrophage-neutrophil interplay was not necessary for neutrophil efflux in that study, demonstrating that other factors and mechanisms are involved in this process [40, 41]. Neutrophils are able to reenter the blood stream by passing endothelial cells.…”

Section: Leukocyte Egress From Established Atherosclerotic Plaquesmentioning

confidence: 99%

“…Neutrophil reverse transendothelial migration and reentering into the circulation is encouraged by macrophage interaction via redox-regulated Src family kinase signaling in response to reactive oxygen species [40]. Moreover, macrophage-depletion shows an increased number of neutrophils under inflammatory conditions, pointing to uncontrolled neutrophil recruitment.…”

Section: Leukocyte Egress From Established Atherosclerotic Plaquesmentioning

confidence: 99%

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The Ins and Outs of Myeloid Cells in Atherosclerosis

Schumski¹,

Döring²,

Soehnlein³

2018

J Innate Immun

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Atherosclerosis is a chronic inflammation of the arterial vessel wall that arises from an imbalanced lipid metabolism. A growing body of literature describes leukocyte recruitment as a critical step in the initiation and progression of lesion development. By contrast, the role of leukocytes during plaque regression has been described in less detail. Leukocyte egress might be an important step to resolving chronic inflammation and therefore it may be a promising target for limiting advanced lesion development. This review aims to summarize our current knowledge of leukocyte recruitment to the arterial vessel wall. We will discuss mechanisms of leukocyte egress from the lesion site, as well as potential therapeutic strategies to promote atherosclerotic regression.

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Section: Leukocyte Egress From Established Atherosclerotic Plaquesmentioning

confidence: 99%

Section: Leukocyte Egress From Established Atherosclerotic Plaquesmentioning

confidence: 99%

The Ins and Outs of Myeloid Cells in Atherosclerosis

Schumski¹,

Döring²,

Soehnlein³

2018

J Innate Immun

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“…In zebrafish, the H 2 O 2 gradient not only recruits neutrophils at the wound but also macrophages. Macrophage migration toward the wound site is dependent of the SRC family Kinase, Yes-related kinase that may acts as a sensor for H 2 O 2 [35] .…”

Section: Role Of Macrophages In Wound Healingmentioning

confidence: 99%

“…Direct contacts between macrophages and living neutrophils resulting in some cases with the transfer of cytoplasm portions from neutrophil to macrophage were also shown [36] . More recently, macrophages-neutrophils direct interactions in response to tissue injury were described to promote neutrophilic resolution through a process of neutrophil reverse migration [35] .…”

Section: Role Of Macrophages In Wound Healingmentioning

confidence: 99%

“…Therefore, innovative strategies which seek to deplete macrophages or modulate their functions could be developed in order to alter the outcome of the diseases. [33,51] mpeg1: GAL4 macrophage express 1 promoter, macrophage reporter line [36] mpeg1: kaede macrophage express 1 promoter, macrophage reporter line with photoconvertible fluorescent protein [35] csf1r:GAL4 macrophage colony stimulating factor (fms) reporter line which marks both macrophages and xanthophores [53] mfap4:tdTomato microfibrillar-associated protein 4 promoter, macrophage reporter line [54] Transgenic reporter lines to visualize macrophage subsets and activation irg1:EGFP immunoresponsive gene 1 reporter line, which marks activated macrophages [50] tnfa: GFP-F tumor necrosis factor a reporter line, which marks M1-Like polarized macrophages [51] Transgenic lines to ablate macrophage mpeg1:GAL4/ UAS:nfsb-mCherry Escherichia coli enzyme nitroreductase expression in macrophage, inducible ablation of macrophages [55] mpeg1:nfsb-eYFP Escherichia coli enzyme nitroreductase expression in macrophage, inducible ablation of macrophages [47] csf1r:GAL4 / UAS:nfsb-mCherry Escherichia coli enzyme nitroreductase expression in macrophage, inducible ablation of macrophages [53,56] Other methods for macrophage ablation MO PU. 1 Decrease of macrophage number with increase of neutrophil number [36,60] …”

Section: Introductionmentioning

confidence: 99%

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Deciphering the complexity of macrophage biology and function with the zebrafish model

Nguyen-Chi¹,

Laplace-Builhé²,

Jorgensen³

et al. 2016

Macrophage

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Macrophages are present in every tissue of the body. Acting as sentinels of the immune system, they have the ability to engulf apoptotic cells and pathogens and also produce effector signals to mount a proper immune response. In response to tissue injury or microbe invasion, they are rapidly recruited to the injured site and are main key players in the protection of the host. Associated with many diseases, macrophages can have deleterious roles, especially due to their pro-inflammatory function. However, macrophages were discovered to be central during the orchestration of every step of inflammation, from initiation to resolution phases and to participate in tissue development, homeostasis and repair. These plural functions exerted by macrophages support their high plasticity and versatility potential and suggest the existence of macrophage subsets that might be differentially activated and/or recruited during physiological and pathological processes. The study of macrophage behaviour dynamics and functions in their activated states requires tractable in vivo models in which macrophages can be visualized under physiological or stress conditions. Thus, the zebrafish (Danio rerio) has emerged as an excellent vertebrate system to study myeloid development, inflammation and host-pathogen interactions. Conservation of immune cell lineage, optical accessibility of the zebrafish embryo combined with genetic approaches unable us to improve our understanding of macrophage functions. In this review, we discuss recent studies that have used the zebrafish advantages to provide key advances in the field of vertebrate macrophage biology and functions.

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Tracing Immunological Interaction in Trimethylamine N‐Oxide Hydrogel‐Derived Zwitterionic Microenvironment During Promoted Diabetic Wound Regeneration

Li,

Yue

et al. 2024

Advanced Materials

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The diabetic wound healing is challenging due to the sabotaged delicate balance of immune regulation via an undetermined pathophysiological mechanism, so it is crucial to decipher multicellular signatures underlying diabetic wound healing and seek therapeutic strategies. Here, this work develops a strategy using novel trimethylamine N‐oxide (TMAO)‐derived zwitterionic hydrogel to promote diabetic wound healing, and explore the multi‐cellular ecosystem around zwitterionic hydrogel, mapping out an overview of different cells in the zwitterionic microenvironment by single‐cell RNA sequencing. The diverse cellular heterogeneity is revealed, highlighting the critical role of macrophage and neutrophils in managing diabetic wound healing. It is found that polyzwitterionic hydrogel can upregulate Ccl3+ macrophages and downregulate S100a9+ neutrophils and facilitate their interactions compared with polyanionic and polycationic hydrogels, validating the underlying effect of zwitterionic microenvironment on the activation of adaptive immune system. Moreover, zwitterionic hydrogel inhibits the formation of neutrophil extracellular traps (NETs) and promotes angiogenesis, thus improving diabetic wound healing. These findings expand the horizons of the sophisticated orchestration of immune systems in zwitterion‐directed diabetic wound repair and uncover new strategies of novel immunoregulatory biomaterials.

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Redox and Src family kinase signaling control leukocyte wound attraction and neutrophil reverse migration

Abstract: Redox and Src family kinase signaling in tissue adjacent to a wound coordinates initial attraction of leukocytes and the subsequent repulsion of neutrophils following contact with macrophages to resolve inflammation.

Cited by 116 publications

References 32 publications

The Ins and Outs of Myeloid Cells in Atherosclerosis

The Ins and Outs of Myeloid Cells in Atherosclerosis

Deciphering the complexity of macrophage biology and function with the zebrafish model

Tracing Immunological Interaction in Trimethylamine N‐Oxide Hydrogel‐Derived Zwitterionic Microenvironment During Promoted Diabetic Wound Regeneration

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