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both organs. The hypothalamus-pituitary-adrenal axis antagonizes GLHs, and sup-
presses adaptive immunity and inflammation. Catecholamines also suppress adap-
tive immunity through their beta-adrenergic receptors, and stimulate NATIM. During
homeostasis, NATIM and ADIM are well balanced. Some immune functions, such as
surface receptor expression, are promoted by glucocorticoids (GCs; part of NATIM).
Physiological levels of GCs were found to be necessary for normal immune function.
Other steroids, thyroid hormones, and vitamin D also modulate immune function, by
either enhancement or suppression. Neuropeptides (NPEPs) play a major role in reg-
ulating neurogenic inflammation, though they also modulate immunity. NPEPs also
have a role in feedback signaling to the CNS, along with cytokines and chemokines
[18,23] .
Glucocorticoids and beta-2 adrenergic agonists induce interleukin-10-secreting
regulatory/suppressor T cells (Tsrs) in vitro from peripheral blood leukocytes of
allergic patients [34] . It has long been established that elevated levels of glucocorti-
coids suppress adaptive immunity [35] . More recently, it became apparent that physi-
ological levels of glucocorticoids are needed for T lymphocyte development and
function [36] . Elevated levels of glucocorticoids and catecholamines stimulate Tsr
development and also amplify NATIM during acute illness [16] .
7.2.6 Acute Illness
During acute febrile illness (in which an acute phase response or APR is mounted),
the hypothalamus is activated by IL-1, -6, and TNF- to secrete corticotropin-
releasing hormone (CRH) and vasopressin (VP), which act on the pituitary gland and
indeed on the entire organism. Growth and lactogenic hormones are suppressed, the
thymus is involuted, and the entire ADIM system is suppressed. The HPA axis is acti-
vated and regulatory/suppressor T cells are stimulated by GCs and catecholamines
(CATs). Because Tsr is amplified by DC and CATs, we suggest that it has the char-
acteristics of innate immune cells. The bone marrow is stimulated by IL-6, colony-
stimulating factors (CSFs), insulin (INS), and leptin (LEP). The liver is induced to
produce acute phase proteins (APP) by IL-6, GCs, and CATs. The cytokines (primar-
ily IL-1) induce fever, whereas alpha-melanocyte stimulating hormone (MSH) acts
as a suppressor of fever. Catabolism and lipolysis (brought about by TNF and leptin)
prevail in the body when the CNS, pituitary, leukocytes, and bone marrow are stimu-
lated. Insulin resistance and hyperglycemia (induced by IL-1, TNF, and GCs) occur
in a response aimed at nourishing the defense system of the body. The GLH-IGF
(insulin-like growth factor) axis is replaced by INS, glucagon, and leptin. Cholinergic
agents are anti-inflammatory during APR [16,37,38] .
The APR is an excellent example of the regulatory power of the hypothalamus
in emergency situations, in which a rapid response can be life-saving. The profound
neuroendocrine and metabolic response generated by the neuroimmune system
in response to infection (or trauma) suppresses ADIM, which needs a long time to
act, and rapidly amplifies NATIM, which is ready to act instantaneously against the
infecting (causative) agent. This defense strategy usually works very well; most of us
have had febrile illnesses and recovered numerous times during our lifetimes.
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