Brain, Behavior, and Immunity 20 (2006) 94–95
Conference Report of the 4th Symposium of the German-
inhibits T-cell activation by targeting the calcineurin path-
Endocrine–Brain–Immune Network together with the German
way. Ha¨rle et al., Rheumatology, Regensburg, demonstrat-
Zoological Society, Bayreuth, Germany, October 3–6, 2005
ed novel effects of the peripheral sympathetic nervoussystem on CD4+CD25+ T-cells in the collagen-induced
The 4th Symposium of the German Endocrine Brain
arthritis model. He showed that the sympathetic nervous sys-
Immune Network (GEBIN) was held from October 3rd un-
tem stimulates a proinflammatory phenotype of these cells.
til 6th at the campus of the University of Bayreuth, Bavar-
In the session on neuroendocrinology and immune func-
ia, Germany. As a special of this meeting, the symposium
tions, Kraus et al., Pharmacology and Toxicology, Magde-
was held together with the 98th Congress of the German
burg, demonstrated a novel interaction of the opioid and
Zoological Society (GZS) in order to intensify the network
cannabinoid system in Jurkat T-cells. He demonstrated
how cannabinoids signal via STAT5 to upregulate IL-4secretion. He showed, by using transcription factor decoy
1. The plenary sessions together with the German Zoological
oligonucleotides, that IL-4 transactivates the l-opioid
receptor gene via STAT6. This cooperative effect of bothsystems may contribute to the analgesic effect of cannabi-
In two outstanding plenary talks, Robert Dantzer, Bor-
noids. Beat Lutz, Max Planck Institute for Psychiatry, Mu-
deaux, France, and Shamgar Ben-Eliahu, Tel Aviv, Israel,
nich, demonstrated how the cannabinoid system is
summarized their extensive research. Robert Dantzer
important to normalize and maintain the bodyÕs homeosta-
bridged the important gap between sickness behavior on
sis. He showed that endogenous cannabinoids trigger obes-
one side and depression on the other. He presented con-
ity and that antagonists to endogenous cannabinoid
vincing arguments that systemic and CNS-borne cytokines
play an extremely important role for both entities. Sham-
Capellino et al., Rheumatology, Regensburg, demon-
gar Ben-Eliahu demonstrated important links between
strated that different estrogen metabolites have opposing
the stress system and tumor metastasis. His research lead
effects on an immune response. She showed that 16a-, 4-,
to the evolution of novel therapeutic strategies to inhibit
and 2-hydroxyesterone confer anti-proliferative effects
surgery—associated stress which might decrease sur-
and that 2-hydroxyestradiol exerts mitogenic effects in acti-
gery—associated metastatic spreading.
vated human monocytic cells at low concentrations of10À9–10À11 mol/l. A local dysregulation of estrogen metab-
2. Peripheral neuroendocrine immune connections
olism in chronic synovitis in rheumatoid arthritis patientsmight be involved in the pathogenesis of this disease. Orsal
In the more specific part of the GEBIN meeting, Jo¨rg
et al., Psychosomatic Clinic, Berlin, reported on the influ-
Reichrath, Dermatology, Homburg, demonstrated immu-
ence of progesterone derivatives on neurogenic inflamma-
nomodulatory effects of 1,25-dihydroxyvitamin D, deriva-
tion. Dydrogesterone induced a decrease in NK-cells and
tives thereof, and their anti-proliferative and differentiating
an increase of Th2 cytokines by decreasing Th1 cytokines.
effects. In addition, these hormones can generate tolerance
These studies gave a good example for the cross-talk of the
via CD4+CD25+ T-cells. Furthermore, he showed that im-
nervous, endocrine, and immune system during inflamma-
mune cells have the potential to locally produce biologically
activate vitamin D, which feeds-back on immune cells by the
Several reports were devoted to allergic skin diseases.
Daniltchenko et al., Psychosomatic Clinic, Berlin, demon-
In the session relating to peripheral neuroimmune interac-
strated an impact of stress on the worsening of dermatitis
tions, Fiebich et al., Psychiatry, Freiburg, provided new
via alteration of neurogenic inflammation and the hypotha-
mechanistic insights into the anti-inflammatory activities
lamic–pituitary-axis (HPA)-activation. Rohleder et al.,
of 5-HT3-receptor antagonists such as tropisetron, which
Biopsychology, Dresden, demonstrated an alteration of
Conference report / Brain, Behavior, and Immunity 20 (2006) 94–95
the cortisol response and glucocorticoid sensitivity in
trated in animal models how effective glucocorticoids in a
atopic men and women during stressful conditions.
liposomal formulation can achieve high tissue concentra-
Bo¨hm et al., Dermatology, Mu¨nster, reported how the
tions thus greatly reducing local immunopathology in
a-MSH system links the endocrine and the immune system.
arthritis. This therapeutic intervention may be useful dur-
He showed data, that human basophils express functional
ing flare-ups of arthritis and encephalomyelitis. Dimitrov
receptors for the neuropeptide a-MSH, which inhibits
et al., Neuroendocrinology, Lu¨beck, demonstrated how
expression of IL-4. Moreover, in a murine model of allergic
sleep can modulate the immune response by increasing
airway inflammation, systemic treatment with a-MSH
IL-12 production form pre-myeloid dendritic cell precur-
resulted in a significant reduction of allergen-specific IgE
sors. Schwarz et al., Psychiatry, Munich, reported an
production, eosinophil influx, and IL-4 production.
over-stimulation of the tryptophan degrading enzyme(IDO) mediated by proinflammatory cytokines in patientswith depressive disorders. Mu¨ller and Riedel et al., Psychi-
atry, Munich, demonstrated that inhibition of COX-2 con-fers an anti-inflammatory effect via the inhibition of
Niemi and Pacheco-Lopez et al., Psychology and Behav-
prostaglandin E2 and pro-inflammatory cytokines. They
ioral Immunobiology, Zu¨rich, demonstrated how the im-
pointed out that COX-2 inhibition has therapeutic effects
in early stages of schizophrenia and in depression. Musil
conditioning model with cyclosporin A, they demonstrated
et al., Psychiatry, Munich, demonstrated that macrophage
how the human immune system can ‘‘learn immunosup-
inhibitory factor (MIF) is significantly elevated in de-
pression’’ by a conditioned stimulus. They also indicated
pressed patients. MIF is secreted by the pituitary gland
that the insular cortex is the most important brain area
together with ACTH. The significance of up-regulated
for these effects. Knackstedt et al., Pediatrics, Berlin, dem-
MIF levels is not yet clear but might be a factor for in-
onstrated how maternal stress may increase the susceptibil-
creased circulating cytokines in these diseases. Mu¨ller, Psy-
ity towards a Th2-driven immune response thus rendering
chiatry, Munich, summarized the growing evidence that
mice to a higher risk for atopic diseases like asthma in off-
central inflammatory mechanisms play an important role
springs. Reber et al., Zoology, Regensburg, provided evi-
in the long-term neurodegenerative changes in depression
dence that chronic social stress in mice decreases the
by inducing neuronal apoptosis and exciting neurons.
severity of acute colitis, which was followed by impaired
Thanks to the excellent organization of Volker Stefanski
wound healing and higher mortality. Engler et al., Psychol-
and Dietrich von Holst not only the scientific program but
ogy and Behavioral Immunobiology, Zu¨rich, showed how
also social aspects of this meeting were admirable (see also
social stress can impair the anti-inflammatory capacity of
glucocorticoids in termination of inflammatory processes. He also found a redistribution of CD11b+ cells from the
bone-marrow to the spleen during social stress. Dawils
et al., Animal Physiology, Bayreuth, demonstrated a nega-
tive impact of acute stressors on the susceptibility to NK-
German-Endocrine–Brain–Immune Network (GEBIN)
sensitive tumor metastasis and how the susceptibility may
be attenuated by different social housing conditions.
Department of Internal Medicine I, University Hospital,
4. Neuroimmune–endocrine network in psychiatric disorders
Metselaar et al., Pharmaceutical Sciences, Utrecht, illus-
Received 21 October 2005; accepted 22 October 2005
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