Immune System Communication with the Nervous System Hormones

There is now convincing evidence to show that the immune system can communicate with the central nervous system (CNS) (Wrona 2006). The invasion of the body by microorganisms activates cells of the immune system, which then releases a complex variety of soluble mediators called cytokines, which include interleukins, interferons, and tumor necrosis factors. These substances modulate the immune response but also influence the brain. This immune-to-brain pathway of communication triggers what we know as the "sickness response." It is this effect which is discussed below and which constitutes the second arm of bidirectional communication.

Cytokines released after infection produce many effects on behavior, including decreased feeding, sexual activity, and pleasure seeking behaviors. In addition, sleep is increased and cognitive function is impaired (Banks, Farr, and Morley 2002). Several mechanisms have been proposed by which blood-borne cytokines convey information to the CNS (Dinarello 2004). These include cytokine acting at the circumventricular organ (CVO), acting at afferent nerves including the vagal, or altering the permeability of the blood-brain barrier (BBB) to immune cells or another substance. In addition to these indirect mechanisms of effects on cytokines on the brain, cytokine transport across the BBB has also been described. The list of cytokine transporters includes IL-1, IL-6, tumor necrosis factor-a, and the IL-1 receptor antagonist (Banks et al. 2002). The cytokine transporters are usually distinguishable from cytokine receptors and interestingly show differences in regional uptake in the brain (Banks, Moinuddin, and Morley 2006). It appears that in the case of fever, exogenous pyrogens (bacterial products and foreign antigens), and endogenous pyrogens (cytokines) from the circulation bind to Toll-like receptors (TLR) and cytokine receptors in the CVO, respectively. Activation of TLR and/or cytokine receptors induces cyclooxygenase-2, which results in the synthesis of prostaglandin-E2 (PGE2) on the brain side of the CVO (Dinarello 2004). The increases in PGE2 stimulate the release of cAMP and other neurotransmitters triggering neurons in the thermoregulatory center as well as initiating behavioral responses. Interestingly, fever in autoimmune diseases appears to be mostly cytokine-mediated whereas fever during infection may be both cytokine- and TLR-mediated (Dinarello 2004).

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