Nerve growth factor enhances survival and cytotoxic activity of human eosinophils

Hamada, Atsuo; Watanabe, Naohiro; Ohtomo, Hiroshi; Matsuda, Hiroshi

doi:10.1046/j.1365-2141.1996.5151055.x

Cited by 84 publications

(50 citation statements)

References 16 publications

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“…NGF has been demonstrated as an important factor for hematopoietic colony growth and differentiation [41]. Previous work documents its ability to directly influence proliferation, differentiation, and maturation of myeloid progenitors along with induction of migration, survival and activation of mature hematopoietic cells [42][43][44]. NGF is also a chemotactic stimulus for human leukocytes and macrophages [45,46].…”

Section: Discussionmentioning

confidence: 99%

“…As such, neurotrophins are positioned to regulate the availability of inflammatory cells derived from the marrow, through both direct [41][42][43][44] and indirect mechanisms. Taken together, our data suggest a central role for neurotrophins in the inflammatory process subsequent to infection and identify bone marrow stroma as a novel target for these factors.…”

Section: Discussionmentioning

confidence: 99%

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Neurotrophins Regulate Bone Marrow Stromal Cell IL-6 Expression through the MAPK Pathway.

Rezaee¹,

Rellick²,

Akers³

et al. 2009

B33. Immunology/Inflammation

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Background: The host's response to infection is characterized by altered levels of neurotrophins and an influx of inflammatory cells to sites of injured tissue. Progenitor cells that give rise to the differentiated cellular mediators of inflammation are derived from bone marrow progenitor cells where their development is regulated, in part, by cues from bone marrow stromal cells (BMSC). As such, alteration of BMSC function in response to elevated systemic mediators has the potential to alter their function in biologically relevant ways, including downstream alteration of cytokine production that influences hematopoietic development.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neurotrophins Regulate Bone Marrow Stromal Cell IL-6 Expression through the MAPK Pathway.

Rezaee¹,

Rellick²,

Akers³

et al. 2009

B33. Immunology/Inflammation

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“…The study results suggest that anti-NGF antibodies block the effects of NGF on the periphery of the nervous system and suppress epidermal innervation, dermatitis, and scratching behavior. There is also growing evidence that NGF has biological effects on immune cells, such as mast cells (34), B cells (35), T cells (36), neutrophils (37), eosinophils (38), and basophils (39). Anti-NGF antibodies may suppress these symptoms in NC / Nga mice by blocking response to these immune cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of Anti-Nerve Growth Factor Antibody on Symptoms in the NC/Nga Mouse, an Atopic Dermatitis Model

2005

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Abstract. Nerve growth factor (NGF) is an important substance in the skin, where it can modulate nerve maintenance and repair. However, the direct link between NGF and pruritic disease such as atopic dermatitis is not yet fully understood. To determine whether NGF plays a major role in atopic dermatitis and in the development or maintenance of skin lesions, we performed a study using NC / Nga mice and compared mice with and without skin lesions. Our examinations of the NC / Nga mice sought to detect nerve fibers in the epidermis, measured serum and skin NGF content, and observed skin NGF by immunohistochemistry staining. We also examined the effects of anti-NGF antibody on dermatitis symptoms in NC / Nga mice. In these mice, nerve fibers were significantly increased in the epidermis of lesioned skin, and the NGF content of the serum and skin was significantly elevated. Anti-NGF antibodies significantly inhibited the development and proliferation of skin lesions and epidermal innervation and significantly inhibited any growth in scratching but did not ameliorate scratching already developed. Our findings suggest that NGF plays important roles in the pathogenesis of atopic dermatitis-like skin lesions and that inhibiting the physiological effects of NGF or suppressing increased NGF production may prevent or even moderate the symptoms of atopic dermatitis.

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“…In prior studies, we have demonstrated that NGF promotes not only granulocyte differentiation from human PBMC and murine bone marrow cells (12,13), but also differentiation of connective tissue-type mast cells from murine bone marrow cells and bone marrow-derived culture mast cells (14). NGF is capable of supporting survival of neutrophils (15), eosinophils (16), and mast cells (9) by preventing apoptosis, and enhancing functional properties of neutrophils, eosinophils, macrophages, and mast cells: phagocytosis, superoxide production, matrix metalloproteinase-9 production, and chemotaxis (11, 12, 16 -20). These experimental findings strongly support a possibility that NGF acts as a cytokine that is capable of modulating inflammatory responses and tissue repair.…”

Section: N Erve Growth Factor (Ngf)mentioning

confidence: 99%

Nerve Growth Factor Activates Mast Cells Through the Collaborative Interaction with Lysophosphatidylserine Expressed on the Membrane Surface of Activated Platelets

Kawamoto

Aoki

Tanaka

et al. 2002

The Journal of Immunology

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Effect of nerve growth factor (NGF) on platelet-associated mast cell activation was investigated. Although neither NGF alone nor platelets alone induced significant 5-hydroxytriptamine (5-HT) release from rat peritoneal mast cells, marked 5-HT release was detected when costimulated with NGF and calcium ionophore-activated platelets. This response reached maximal levels as early as 5 min after the initiation of the coincubation and was completely blocked by anti-NGF Ab or by an inhibitor for a tyrosine kinase of the trkA NGF receptor. Paraformaldehyde-fixed platelets activated with either calcium ionophore or thrombin exhibited the collaborative ability, suggesting the possible involvement of some membrane molecules expressed on activated platelets in mast cell activation. Because activation of platelets induced expression of phosphatidylserine (PS) and/or lysoPS on membrane surface, and since lysoPS, unlike PS, initiated the NGF-induced 5-HT release, lysoPS expressed on activated platelets may be involved in the mast cell activation. Moreover, intradermal injection of NGF and activated platelets into the rat skin increased local vascular permeability. These findings suggested that NGF collaboratively worked with membrane lysoPS of activated platelets to induce mast cell activation. Thus, NGF released in response to inflammatory stimuli may contribute to mast cell activation in collaboration with locally activated platelets in the process of inflammations and tissue repair.

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Nerve growth factor enhances survival and cytotoxic activity of human eosinophils

Cited by 84 publications

References 16 publications

Neurotrophins Regulate Bone Marrow Stromal Cell IL-6 Expression through the MAPK Pathway.

Neurotrophins Regulate Bone Marrow Stromal Cell IL-6 Expression through the MAPK Pathway.

Effects of Anti-Nerve Growth Factor Antibody on Symptoms in the NC/Nga Mouse, an Atopic Dermatitis Model

Nerve Growth Factor Activates Mast Cells Through the Collaborative Interaction with Lysophosphatidylserine Expressed on the Membrane Surface of Activated Platelets

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