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and IL-6 secretion in the spleen
* Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I;
Institute for Medical Microbiology; and the
§ Institute of Pathology/Immunology, University of Regensburg, 93042 Regensburg, Germany
1Correspondence: Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University of Regensburg, Franz Josef Strauss Allee 11, 93042 Regensburg, Germany. E-mail: rainer.straub{at}klinik.uni-regensburg.de
It is believed that an inflammation-induced activation of the CNS leads
to an inhibition of overshooting immune responses to prevent extensive
local cytokine secretion. However, immunosuppression by the sympathetic
nervous system may be unfavorable when bacteria are present locally and
when TNF-
is necessary to overcome infection. We now report in a
superfusion model, using mouse spleen slices, that although local
Pseudomonas aeruginosa increased splenic TNF- and
IL-6 secretion severalfold over basal levels, electrically released
neurotransmitters attenuated cytokine secretion to similar basal level
as under bacteria-free conditions. Bacteria reversed noradrenergic
inhibitory effector mechanisms: Under bacteria-free conditions, TNF-
secretion was very low and IL-6 secretion was mainly inhibited by
2-adrenoreceptor ligation. In the presence of bacteria, TNF- and
IL-6 secretion were high and IL-6 secretion was mainly inhibited by
ß-adrenoreceptor ligation. The - to ß-adrenoswitch of IL-6
inhibition in the presence of bacteria was mediated by the prior
adrenergic regulation of TNF-. In vivo, chemical
abrogation of sympathetic inhibition reduced accumulation of bacteria
in the spleen, which depended at least in part on TNF-. This
suggests that activation of the sympathetic nervous system may be a
forerunner for accumulation of bacteria in tissue and consecutively
sepsis due to intensified inhibition of TNF- secretion.—Straub,
R. H., Linde, H.-J., Männel, D. N., Schölmerich,
J., Falk, W. A bacteria-induced switch of sympathetic effector
mechanisms augments local inhibition of TNF- and IL-6 secretion in
the spleen.
Key Words: Pseudomonas aeruginosa • macrophage • tumor necrosis factor • interleukin 6 • norepinephrine • adrenoreceptor
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