[Brain signaling mechanisms during neonatal sepsis]

Abstract

The brain and the immune system are the two major adaptive systems of the body. During an immune response the developing neonatal brain and the immune system "cross-talk" and this course of action is essential for maintaining homeostasis. Two pathway are involved in this intercommunication: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence suggests that norepinephrine (NE) is a neurotransmitter/neuromodulator in different organs and tissues. Under stimulation, NE is released from the sympathetic nerve terminals in these organs and tissues .Through stimulation of specific receptors, locally released NE, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. In addition, recent evidence is discussed that NE and epinephrine, through stimulation of the beta(2)-adrenoreceptor-cAMP-protein kinase A pathway, inhibit the production of type 1/proinflammatory cytokines, such as interleukin (IL-12), tumor necrosis factor-alpha, and interferon-gamma by antigen-presenting cells and T helper (Th) 1 cells, whereas they stimulate the production of type 2/anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta. Thus, the activation of SNS during an immune response might be aimed to localize the inflammatory response.