The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

Burdon, Peter C. E.; Martin, Coralie; Rankin, Sara M.

doi:10.1182/blood-2004-08-3193

Cited by 91 publications

(100 citation statements)

References 34 publications

(42 reference statements)

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“…Several adhesion molecules, such as integrin subunit α4 (ITGA4) and vascular cell adhesion molecule 1 (VCAM1), as well as some proteases are also important in neutrophil retention [39][40][41] . In addition to its positive influence on granulopoiesis, G-CSF is a well-known disruptor of neutrophil retention 42 .…”

Section: Neutrophil Retention and Release From Bone Marrowmentioning

confidence: 99%

“…Mature cells are retained in the bone morrow by an interplay between two C-X-C chemokine receptors, CXCR4 and CXCR2. Constitutive CXCL12 expression by 4 osteoblasts and other bone marrow stromal cells tether CXCR4 + neutrophils in the bone marrow, whereas secretion of CXCL1 and CXCL2 by endothelial cells and megakaryocytes encourage the release of neutrophils into the circulation via CXCR2 signaling [33][34][35][36][37][38] (Figure 1).Several adhesion molecules, such as integrin subunit α4 (ITGA4) and vascular cell adhesion molecule 1 (VCAM1), as well as some proteases are also important in neutrophil retention [39][40][41] . In addition to its positive influence on granulopoiesis, G-CSF is a well-known disruptor of neutrophil retention 42 .…”

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confidence: 99%

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Neutrophils in cancer: neutral no more

2016

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SummaryNeutrophils are indispensable antagonists of microbial infection and facilitators of wound healing. In the cancer setting, a newfound appreciation for neutrophils has come into view.The traditionally held belief that neutrophils are inert bystanders is being challenged by recent literature. Emerging evidence indicates that tumors manipulate neutrophils, sometimes early in their differentiation process, to create diverse phenotypic and functional polarization states able to alter tumor behavior. In this Review, we discuss the involvement of neutrophils in cancer initiation and progression, and their potential as clinical biomarkers and therapeutic targets. 2The name neutrophil -given to polymorphonuclear, granulocytic cells by Paul Ehrlich in the late 19th century -is based on the inability of these cells to retain acidic or basic dyes and for their preferential uptake of pH neutral dyes 1 . Although their neutral staining led to the identification of these cells, neutrophils in the cancer setting are anything but neutral.Neutrophils in tumor-bearing hosts can oppose or potentiate cancer progression. These two types of behavior are controlled by signals emanating from cancer cells or stromal cells within the tumor microenvironment, which educate neutrophils to execute the demise of the tumor or facilitate support networks that lead to its expansive spread. These functions can occur locally in or around the tumor microenvironment, as well as systemically in distant organs.Until the past few years, other immune cells such as macrophages have overshadowed the role of neutrophils in cancer. But recent studies and the development of new genetic tools have provided the cancer community with new insights into the profound influence of these dynamic cells by uncovering distinct capabilities for neutrophils throughout each step of carcinogenesis: from tumor initiation to primary tumor growth to metastasis.During these processes, neutrophils take on different phenotypes and sometimes opposing functions. Emerging evidence also indicates that these cells are highly influential, and are able to change the behavior of other tumor-associated cell types -primarily other immune cells. In this Review, we focus on how tumors manipulate the generation and release of neutrophils from the bone marrow. We discuss the mechanisms identified in animal models by which neutrophils participate in tumor initiation, growth and metastasis. Finally, we highlight the potential of these cells as clinical biomarkers and therapeutic targets. In humans, neutrophils are the most abundant immune cell population, representing 50-70% of all leukocytes. Over 10 11 neutrophils may be produced per day 2 , and tumors can increase this number by even more. Indeed, patients with various cancer types, including but not limited to breast, lung and colorectal cancer, often exhibit increased numbers of circulating neutrophils 3,4 . Recent studies have identified key pathways that tumors exploit to disrupt normal neutrophil homeostasis and these are discuss...

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Section: Neutrophil Retention and Release From Bone Marrowmentioning

confidence: 99%

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confidence: 99%

Neutrophils in cancer: neutral no more

2016

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“…The in situ perfusion technique of the femoral bone marrow was used as previously described (Palframan et al, 1998a,b;Burdon et al, 2005). Briefly, rats were anaesthetized and the external iliac artery and veins were exposed.…”

Section: In Situ Perfusion Of the Rat Hind Limbmentioning

confidence: 99%

“…Erythrocytes present in the cell pellet were lysed using FACS TM lyse and the leucocytes were then resuspended in FACS TM counting buffer for quantification of leucocyte numbers by flow cytometry. Cell counts were obtained by gating on the different leucocyte populations and the fluorospheres and acquiring events for a set time period of 30 s as previously described (Burdon et al, 2005).…”

Section: In Situ Perfusion Of the Rat Hind Limbmentioning

confidence: 99%

“…Thus, mechanistically, mobilization would involve a detachment step, as neutrophils are released from the ablumenal surface of the bone marrow sinusoidal endothelium. We have previously shown that CXC chemokines (rat MIP and KC) can selectively mobilize neutrophils from the bone marrow (Burdon et al, 2005). We propose an alternate model whereby chemokine-driven mobilization of neutrophils is due to an elevation in the concentration of neutrophilselective chemokines in the bone marrow sinusoids creating a chemotactic gradient across the sinus wall, directly stimulating neutrophil release from the haematopoietic compartment.…”

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Migration across the sinusoidal endothelium regulates neutrophil mobilization in response to ELR + CXC chemokines

2008

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SummaryAn increase in circulating neutrophils is a characteristic feature of many inflammatory reactions and is a result of the rapid mobilization of neutrophils from the bone marrow, driven by inflammatory mediators, including the ELR + CXC chemokines. In this paper, using a combination of light and electron microscopy and an in situ perfusion system of the rat femoral bone marrow, we examined this mobilization process in detail. We show that mobilization of neutrophils stimulated by the CXC chemokine, rat MIP‐2, involves neutrophil migration from the haematopoietic compartment of the bone marrow across the bone marrow sinusoidal endothelium via a transcellular route. The critical role of the bone marrow sinusoidal endothelium in regulating neutrophil mobilization was demonstrated by artificially disrupting the bone marrow endothelial barrier by treatment with cytochalasin D, which results in the non‐selective release of leucocytes from the bone marrow. In contrast, inhibiting the activity of p38 mitogen‐activated protein kinase, inhibited both MIP‐2 stimulated chemotaxis of bone marrow neutrophils in vitro and neutrophil mobilization in situ while, a broad spectrum matrix metalloproteinase inhibitor, BB94, had no effect on neutrophil mobilization. These results support the hypothesis that neutrophil migration drives their mobilization and highlights the function of the sinusoidal endothelium in regulating this process.

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Annexin A1 Is a Physiological Modulator of Neutrophil Maturation and Recirculation Acting on the CXCR4/CXCL12 Pathway

et al. 2016

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Neutrophil production and traffic in the body compartments is finely controlled, and the strong evidences support the role of CXCL12/CXCR4 pathway on neutrophil trafficking to and from the bone marrow (BM). We recently showed that the glucocorticoid-regulated protein, Annexin A1 (AnxA1) modulates neutrophil homeostasis and here we address the effects of AnxA1 on steady-state neutrophil maturation and trafficking. For this purpose, AnxA1(-/-) and Balb/C wild-type mice (WT) were donors of BM granulocytes and mesenchymal stem cells and blood neutrophils. In vivo treatments with the pharmacological AnxA1 mimetic peptide (Ac2-26) or the formyl peptide receptor (FPR) antagonist (Boc-2) were used to elucidate the pathway of AnxA1 action, and with the cytosolic glucocorticoid antagonist receptor RU 38486. Accelerated maturation of BM granulocytes was detected in AnxA1(-/-) and Boc2-treated WT mice, and was reversed by treatment with Ac2-26 in AnxA1(-/-) mice. AnxA1 and FPR2 were constitutively expressed in bone marrow granulocytes, and their expressions were reduced by treatment with RU38486. Higher numbers of CXCR4(+) neutrophils were detected in the circulation of AnxA1(-/-) or Boc2-treated WT mice, and values were rescued in Ac2-26-treated AnxA1(-/-) mice. Although circulating neutrophils of AnxA1(-/-) animals were CXCR4(+) , they presented reduced CXCL12-induced chemotaxis. Moreover, levels of CXCL12 were reduced in the bone marrow perfusate and in the mesenchymal stem cell supernatant from AnxA1(-/-) mice, and in vivo and in vitro CXCL12 expression was re-established after Ac2-26 treatment. Collectively, these data highlight AnxA1 as a novel determinant of neutrophil maturation and the mechanisms behind blood neutrophil homing to BM via the CXCL12/CXCR4 pathway. J. Cell. Physiol. 231: 2418-2427, 2016. © 2016 Wiley Periodicals, Inc.

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The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

Cited by 91 publications

References 34 publications

Neutrophils in cancer: neutral no more

Neutrophils in cancer: neutral no more

Migration across the sinusoidal endothelium regulates neutrophil mobilization in response to ELR + CXC chemokines

Annexin A1 Is a Physiological Modulator of Neutrophil Maturation and Recirculation Acting on the CXCR4/CXCL12 Pathway

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