Celsus described four of the five cardinal signs of inflammation 2000 years ago, and Eustachio discovered the adrenal glands almost 500 years ago, but not until 1936 did Selye note that in rats exposed to stressors, the adrenal glands were enlarged, and the thymus and lymph nodes shrunken.1–3 Cortisone, the active principle of the adrenal glands, was isolated by Kendall and Reichstein in the late 1940s and shown to suppress immune organs. These scientists, along with Hench, received the Nobel Prize in Physiology and Medicine, after Hench and colleagues showed that cortisone could ameliorate rheumatoid arthritis.4,5 In recent . . .

The Hypothalamic–Pituitary–Adrenal Axis and Immune-Mediated Inflammation

Turnbull, Andrew V., and Catherine L. Rivier. Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action. Physiol. Rev. 79: 1–71, 1999. — Glucocorticoids a...

Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action

Publisher Summary Interleukin-1 (IL-1) and tumor necrosis factor (TNF) participate in self-augmentation induction mechanisms. Recombinant human IL-1 and TNF are each capable of inducing the production of their respective molecules as well as each other. IL-1 and TNF both induce IL-6. The target cells include: monocytes, endothelial cells, smooth muscle cells, and B cells. The concentrations of IL-1 and TNF that stimulate their own production in this self amplification cycle are within the range (1-10 ng/ml) of what has been measured in the supernatant media of cultured cells stimulated with viruses, bacterial toxins, and active complement components, and of immune complex. The ability of interferon-y to suppress IL-l-induced IL-1 production takes place in the presence of cyclo-oxygenase inhibition. Similarly, the ability of corticosteroids to reduce the transcription of IL-1 messenger RNA (mRNA) also takes place in the presence of cyclooxygenase inhibition. IL-1 is the prototype of a group of biologically potent polypeptides with molecular weights between 10,000 and 30,000. Because these substances are produced by a variety of cells and act on many different cell types, there is a growing acceptance of the terminology “cytokines,” rather than “lymphokines” or “monokines.” Of the various “cytokines,” several share the ability to stimulate or augment cell proliferation, initiate the synthesis of new proteins in a variety of cells, and induce the production of inflammatory metabolites. IL-1 is biologically similar to tumor necrosis factor (TNF), lymphotoxin, IL-6, fibroblast growth factor (FGF), platelet derived growth factor (PDGF), and transforming growth factor- β (TGF-β)

Interleukin-1 and its biologically related cytokines.

The syntax of immune-neuroendocrine communication

IN VERTEBRATES, four major systems of intercellular communication exist: the neural, the endocrine, the neuroendocrine, and the immune system. For many years evidence has accumulated linking the neural, the endocrine, and the neuroendocrine systems, but the immune system was often viewed as essentially autonomous. The enormous recent increase in our knowledge of how the immune system is regulated has led many scientists to postulate that this autonomy may be more apparent than real: that the immune system is subject to endocrine and neural control, and that it exerts, in turn, a reciprocal effect on neuroendocrine systems. In this review we intend to examine the interactions between the immune system and the hypothalamic-pituitary-adrenal (HPA) axis. In the first part of the review we will discuss products and components from the immune system that stimulate or inhibit the HPA axis. These include monokines and lymphokines, i.e. the regulatory secretions of the immune system, and other peptides such as ACT...

J. J. Barbose

Papers

Direct stimulation of the adrenal cortex by interleukin-1.