Cytokine Interactions with Adrenal Medullary Chromaffin Cells

Abstract

It is generally accepted that a bi-directional or reciprocal interaction occurs between the immune and neuroendocrine systems, and that this relationship is important for the appropriate physiological functioning of both systems. Similarly, an imbalance in this relationship may contribute to a number of pathologies, most notably those relating to stress. The aim of this article is to consider the interaction of cytokines with the adrenal medulla, a potentially important player in this relationship. The chromaffin cells of the adrenal medulla release catecholamines and a range of biologically active peptides in response to a wide variety of stress-related signals. A growing body of evidence indicates that this stress response is influenced by, and in turn has influence upon, immune signalling. This brief review will focus primarily on the best-described adrenal medullary active cytokines, namely interferon-α, interleukin-6, interleukin-1α/β and tumour necrosis factor-α. In each case, three key issues will be addressed: the physiologically relevant source of the cytokine; the intracellular signalling events arising from activation of its receptor and finally the cellular consequences of such activation in terms of modulation of gene expression and the secretory output of the chromaffin cells.

Impaired adrenal medullary function in a mouse model of depression induced by unpredictable chronic stress

“…In addition the central regulation through the splanchnic nerve, autocrine/paracrine regulation plays a role in the control of adrenal gland function. Neuropeptides and cytokines secreted by either adrenocortical cells and/or chromaffin cells, regulate catecholamine biosynthetic enzymes (Cavadas et al, 2006(Cavadas et al, , 2001Douglas et al, 2010;Rosmaninho-Salgado et al, 2007, 2009. We indeed observed differential changes in the expression of NPY after 7 and 21 days of UCS.…”

Autoimmune Manifestations in the 3xTg-AD Model of Alzheimer's Disease

“…The accompanying increase in serum levels of pro-inflammatory cytokines [94, 95] may compromise the integrity of the blood-brain barrier [96], accounting for cerebral amyloid angiopathy in AD patients and the 3xTg-AD model [97]. At the same time, circulating cytokines can also activate receptors in the pituitary and adrenal glands [98, 99], thus inducing sustained production of steroids [100] to regulate inflammation [101]. However, the opening of the blood-brain barrier to large immune molecules and sustained binding of steroid hormones to cortical and limbic areas may alter emotional reactivity and induce MCI-like deficits at a prodromal stage of disease development.…”

Detection and Organ-Specific Ablation of Neuroendocrine Cells by Synaptophysin Locus-Based BAC Cassette in Transgenic Mice

“…The diffuse neuroendocrine system (DNES) is composed of NE cells scattered throughout the entire body either as single cells or clusters, such as solitary pulmonary NE cells (PNECs) and neuroepithelial bodies (NEBs) [2], the islets of Langerhans in the pancreas [3], [4], gastrointestinal NE cells [5], [6], dermal NE cells (so-called Merkel cells) [7], adrenal medullary NE cell [8]–[10], and prostate NE cells [11]. PNECs are implicated in regulation of lung maturation and growth, function as oxygen-sensing chemoreceptors and are likely important for lung stem cell niches [2].…”