Sympathetic Neuronal Activation Triggers Myeloid Progenitor Proliferation and Differentiation.
Immunity
; 49(1): 93-106.e7, 2018 07 17.
Article
em En
| MEDLINE
| ID: mdl-29958804
ABSTRACT
There is a growing body of research on the neural control of immunity and inflammation. However, it is not known whether the nervous system can regulate the production of inflammatory myeloid cells from hematopoietic progenitor cells in disease conditions. Myeloid cell numbers in diabetic patients were strongly correlated with plasma concentrations of norepinephrine, suggesting the role of sympathetic neuronal activation in myeloid cell production. The spleens of diabetic patients and mice contained higher numbers of tyrosine hydroxylase (TH)-expressing leukocytes that produced catecholamines. Granulocyte macrophage progenitors (GMPs) expressed the ß2 adrenergic receptor, a target of catecholamines. Ablation of splenic sympathetic neuronal signaling using surgical, chemical, and genetic approaches diminished GMP proliferation and myeloid cell development. Finally, mice lacking TH-producing leukocytes had reduced GMP proliferation, resulting in diminished myelopoiesis. Taken together, our study demonstrates that catecholamines produced by leukocytes and sympathetic nerve termini promote GMP proliferation and myeloid cell development.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Sistema Nervoso Simpático
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Neuroimunomodulação
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Mielopoese
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Diabetes Mellitus
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Células Progenitoras de Granulócitos e Macrófagos
Limite:
Animals
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Female
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Humans
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Male
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article