Estimation of kinetic parameters of neutrophilic, eosinophilic, and basophilic granulocytes in human blood

Steinbach, K.H.; Schick, Peter; Trepel, F.; Raffler, H.; Döhrmann, J.; Heilgeist, G.; Heltzel, W.; Li, K.; Past, Wallace L.; Lange, J. A. van der Woerd-de; Theml, H; Fliedner, Theodor M.; Begemann, Herbert

doi:10.1007/bf01008072

Cited by 72 publications

(45 citation statements)

References 17 publications

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“…Indeed, pioneering work from Mantovani and his colleagues in the 1990s showed that many tumor-associated cytokines prolong neutrophil survival in culture 83 . In line with this, there is evidence that the half-life of circulating neutrophils is extended in cancer patients to 17 hours 84 , which may be the result of pro-survival signaling by G-CSF 20 . A longer life may give neutrophils more time to synthesize new molecules and perform additional effector functions during tumor progression.…”

Section: Neutrophil Lifespanmentioning

confidence: 64%

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 Lifespanmentioning

confidence: 64%

Neutrophils in cancer: neutral no more

2016

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“…12,18 Once in the circulation, eosinophils have a half-life of about 18 hours and a mean blood transit time similar to neutrophils (26 h). 19 …”

Section: Biology Of the Eosinophilmentioning

confidence: 97%

Eosinophilic Granulocytes and Damage-associated Molecular Pattern Molecules (DAMPs)

Lotfi

Lee

Lotze

2007

Journal of Immunotherapy

154

119

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The development of a tumor over many years typically leads to reciprocal alternations in the host and the tumor, enabling tumor growth paradoxically in the setting of substantial necrosis and inflammation. When evaluating a tumor, it is important to assess 3 elements: (1) the quantity and quality of tumor-associated leukocytes, (2) their state of activation, and (3) tumor microenvironment. Peripheral blood eosinophilia and tumor-associated tissue eosinophilia are frequently associated with some tumor types and also found after immunotherapy with IL-2, IL-4, granulocyte-macrophage colony-stimulating factor, and antibody to CTLA-4. Within several tumor types including gastrointestinal tumors, tumor-associated tissue eosinophilia is associated with a significantly better prognosis. The converse is true in other tumor types such as differentiated oral squamous cell carcinoma. On the basis of the emergent data, tumor-associated eosinophils have at least 2 dominant nonoverlapping activities: (1) destructive effector functions potentially limiting tumor growth as well as causing recruitment and activation of other leukocytes, (2) immunoregulative and remodeling activities which suppress immune response and promote tumor proliferation. The mechanism by which eosinophils in particular are recruited into tumor tissue is largely unknown. Candidates for causing eosinophil chemotaxis into tumor tissue are the released damage-associated molecular pattern molecules (DAMPs) including the nuclear protein high mobility group box 1. High mobility group box 1 is released upon necrotic cell death and secreted by many cells, particularly during periods of nutrient, hypoxic, or oxidant stress. This overview on eosinophil biology in the context of cancer and necrosis, introduces intriguing and novel strategies targeting eosinophils to enable more effective biologic therapy for cancer patients.

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“…Eosinophils are present in relatively low numbers in peripheral blood, usually accounting for no more than 5% of the total white blood cell count (33). They have a relatively short blood half-life of approximately 18 h (34). Migration to specific body sites, including the lungs and intestines, is mediated by eosinophil chemoattractants such as eotaxins.…”

Section: Eosinophil Differentiation Maturation Migration Activatiomentioning

confidence: 99%

The Biology of Eosinophils and Their Role in Asthma

2017

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This review will describe the structure and function of the eosinophil. The roles of several relevant cell surface molecules and receptors will be discussed. We will also explore the systemic and local processes triggering eosinophil differentiation, maturation, and migration to the lungs in asthma, as well as the cytokine-mediated pathways that result in eosinophil activation and degranulation, i.e., the release of multiple pro-inflammatory substances from eosinophil-specific granules, including cationic proteins, cytokines, chemokines growth factors, and enzymes. We will discuss the current understanding of the roles that eosinophils play in key asthma processes such as airway hyperresponsiveness, mucus hypersecretion, and airway remodeling, in addition to the evidence relating to eosinophil–pathogen interactions within the lungs.

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Estimation of kinetic parameters of neutrophilic, eosinophilic, and basophilic granulocytes in human blood

Cited by 72 publications

References 17 publications

Neutrophils in cancer: neutral no more

Neutrophils in cancer: neutral no more

Eosinophilic Granulocytes and Damage-associated Molecular Pattern Molecules (DAMPs)

The Biology of Eosinophils and Their Role in Asthma

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