Biology Reference
In-Depth Information
Hans Selye described the stress syndrome in 1936
[8]
. He established that the
hypothalamus-pituitary-adrenal (HPA) axis was involved in mediating the stress
response, which could be induced by various “nocuous” agents. The adrenal gland
was stimulated by stress and the thymus and lymph nodes were involuted by gluco-
corticoids (GCs). He also observed gastrointestinal lesions
[9]
. Subsequently, Selye
concluded that the stress response was a host defense reaction, which he called the
“general adaptation syndrome”
[10]
. These observations clearly implied that the
pituitary gland plays an important role in host defense. While I was in Selye's labo-
ratory, I decided to learn more about the interaction of the pituitary gland and of
the brain with immune host defense. We established that adaptive immune (ADIM)
function is regulated by pituitary hormones: for example, prolactin (PRL) and growth
hormone (GH) stimulated immune function, whereas the HPA axis was inhibitory
and antagonized the stimulatory effect of PRL and GH. Human placental lactogen
(HPL) was as efficient as PRL or GH in restoring ADIM function in this system.
Initially we used young (100 g birth weight) hypophysectomized (Hypox) rats,
and the antigen was always injected without adjuvant 7-10 days after operation.
Treatment of intact animals with the dopamine-agonist drug bromocriptine was
as effective as Hypox in suppressing ADIM function
[11-13]
. Others showed that
immune-derived cytokines (CTKs) are capable of stimulating the HPA axis. This dis-
covery revealed that ADIM function is regulated by the CNS and that the HPA axis,
but also PRL and GH, receive feedback regulatory signals from immune-derived
CTKs
[14,15]
.
Ader and co-workers, and Gorczynski and Kennedy showed that immune function
is subject to Pavlovian conditioning
[16,17]
. These observations imply that the host
is able to activate immune defense when danger is anticipated. However, the mecha-
nisms involved in immune conditioning are complex and poorly understood
[18]
.
1.2 Recent Developments in Neuroimmune Biology
1.2.1 The Concept of Neuroimmune Biology
During the past three decades, the field of neuroimmune interactions grew steadily,
and has now evolved into a sophisticated and credible area of biology. A number of
terms have been proposed to name this multidisciplinary science. Because this sci-
ence deals with the physiology and pathophysiology of higher organisms, in 2000
we coined the term
neuroimmune biology
(NIB)
[19]
, which has been accepted by
the scientific community. It is clear that the CNS, the endocrine system (ES), and
the immune system (IS) form a regulatory circuit, which integrates, coordinates, and
regulates all functions in higher organisms from conception till death.
By now a lot of information has been accumulated about the recognition systems
and signaling in this neuroimmune supersystem (NISS)
[20]
. The mediators for sig-
naling are hormones, neurotransmitters, neuropeptides, CTKs, and chemokines,
which are shared within the NISS. Indeed, sharing occurs throughout the entire organ-
ism, which makes it possible to signal efficiently within the animal or human being.
