Neuroendocrine Control of Macrophage Development and Function

Abstract

Macrophages carry out numerous physiological activities that are essential for both systemic and local homeostasis, as well as innate and adaptive immune responses. Their biology is intricately regulated by hormones, neuropeptides, and neurotransmitters, establishing distinct neuroendocrine axes. The control is pleiotropic, including maturation of bone marrow-derived myeloid precursors, cell differentiation into functional subpopulations, cytotoxic activity, phagocytosis, production of inflammatory mediators, antigen presentation, and activation of effector lymphocytes. Additionally, neuroendocrine components modulate macrophage ability to influence tumor growth and to prevent the spreading of infective agents. Interestingly, macrophage-derived factors enhance glucocorticoid production through the stimulation of the hypothalamic–pituitary–adrenal axis. These bidirectional effects highlight a tightly controlled balance between neuroendocrine stimuli and macrophage function in the development of innate and adaptive immune responses. Herein, we discuss how components of neuroendocrine axes impact on macrophage development and function and may ultimately influence inflammation, tissue repair, infection, or cancer progression. The knowledge of the crosstalk between macrophages and endocrine or brain-derived components may contribute to improve and create new approaches with clinical relevance in homeostatic or pathological conditions.

Crosstalk Between Innate and T Cell Adaptive Immunity With(in) the Muscle

“…In short, inflammatory components such as LPS and cytokines like IL-12, IFN-γ, and TNF-α polarize monocytes and macrophages into a pro-inflammatory population (also known as M1 or classically activated macrophages). Conversely, immunocomplexes, glucocorticoids, and cytokines such as IL-4, IL-13, and IL-10 can induce subpopulation of anti-inflammatory macrophages (known as M2, alternatively activated or regulatory macrophages) (Italiani and Boraschi, 2014;Murray et al, 2014;Vannella and Wynn, 2017;Jurberg et al, 2018).…”

Interaction between stress hormones and phagocytic cells and its effect on the health status of dairy cows: A review

“…Stress in any form, physiological or pathological, causes the release of neuroendocrine signals from the brain. The main two neuroendocrine pathways activated in response to stress and control the immune system are the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) [ 28 , 32 ]. Stimulation of these two systems results in the release of glucocorticoids and catecholamines (epinephrine and norepinephrine), respectively ( Figure-2 ).…”

“…Stress hormones serve as beacons that make the immune system ready for potential challenges perceived by the brain. Nevertheless, the homeostasis of this system may break down if the enhanced immune response is dysregulated after long activation, as seen during chronic stress [ 32 , 33 , 41 , 42 ].…”

Redefining the perioperative stress response: a narrative review

“…127 Glucocorticoids help resolve inflammation by reducing neutrophil extravasation, 125 increasing apoptotic death of neutrophils 128 and augmenting phagocytic activity in tissueresident macrophages. 129 The potential effect of established preoperative disruption of normal glucocorticoid signalling on the orchestration of perioperative inflammation in patients with pre-morbidity linked to HPA axis dysfunction is unclear. 130…”