| Texto completo | |
| Autor(es): |
Freire, Beatriz Marton
;
de Melo, Filipe Menegatti
;
Basso, Alexandre S.
Número total de Autores: 3
|
| Tipo de documento: | Artigo Científico |
| Fonte: | IMMUNOTHERAPY ADVANCES; v. 2, n. 1, p. 12-pg., 2022-06-22. |
| Resumo | |
Macrophages are immune cells that are widespread throughout the body and critical for maintaining tissue homeostasis. Their remarkable plasticity allows them to acquire different phenotypes, becoming able either to fight infection (M1-like, classically activated macrophages) or to promote tissue remodeling and repair (M2-like, alternatively activated macrophages). These phenotypes are induced by different cues present in the microenvironment. Among the factors that might regulate macrophage activation are mediators produced by different branches of the nervous system. The regulation exerted by the sympathetic nervous system (SNS) on macrophages (and the immune system in general) is becoming a subject of increasing interest, indeed a great number of articles have been published lately. Catecholamines (noradrenaline and adrenaline) activate alpha and beta adrenergic receptors expressed by macrophages and shape the effector functions of these cells in contexts as diverse as the small intestine, the lung, or the adipose tissue. Activation of different subsets of receptors seems to produce antagonistic effects, with a adrenergic receptors generally associated with pro-inflammatory functions and beta adrenergic receptors (particularly beta 2) related to the resolution of inflammation and tissue remodeling. However, exceptions to this paradigm have been reported, and the factors contributing to these apparently contradictory observations are still far from being completely understood. Additionally, macrophages per se seem to be sources of catecholamines, which is also a subject of some debate. In this review, we discuss how activation of adrenergic receptors modulates macrophage effector functions and its implications for inflammatory responses and tissue homeostasis. (AU) | |
| Processo FAPESP: | 17/26242-1 - Influência da ativação da sinalização adrenérgica na polarização do macrófago e sua implicância no desenvolvimento/curso da EAE |
| Beneficiário: | Beatriz Marton Freire |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado Direto |
| Processo FAPESP: | 21/11220-8 - Efeito do receptor adrenérgico beta-2 (b2ar) e da proteína Nur77 na reprogramação metabólica de macrófagos |
| Beneficiário: | Beatriz Marton Freire |
| Modalidade de apoio: | Bolsas no Exterior - Estágio de Pesquisa - Doutorado Direto |
| Processo FAPESP: | 16/08180-6 - Estudo da regulação dos inflamassomos exercida pelo Sistema Nervoso Simpático (SNS) |
| Beneficiário: | Filipe Menegatti de Melo |
| Modalidade de apoio: | Bolsas no Brasil - Pós-Doutorado |