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neuroimmune perspectives in sepsis神经免疫角度在脓毒症
Available online /content/13/2/133
Commentary
Neuroimmune perspectives in sepsis
Luis Ulloa and Edwin A Deitch
Department of Surgery, UMDNJ – New Jersey Medical School, 185 South Orange Avenue, PO Box 1709, Newark, NJ 07103, USA
Corresponding author: Luis Ulloa, Mail@LuisU
Published: 23 April 2009 Critical Care 2009, 13:133 (doi:10.1186/cc7758)
This article is online at /content/13/2/133
© 2009 BioMed Central Ltd
See related research by Hofer et al., /content/13/1/R11
Abstract The studies of Hofer and colleagues suggest that central
Physiologic anti-inflammatory mechanisms are selected by sympatholytics may control systemic inflammation by inhibit-
evolution to control the immune system and to prevent infectious ing NF-κB and cytokine production in the liver [1]. If the
and inflammatory disorders. Central-acting α2-agonists attenuate vagus nerve mediates the anti-inflammatory potential of the
systemic inflammation and improve survival in experimental sepsis. α2-agonists, however, central sympatholytics may modulate
This anti-inflammatory and therapeutic mechanism of central sym- systemic inflammation through a mechanism mediated by the
patholytics appears to be mediated by an unexpected vagomimetic spleen [4]. Recent studies indicate that the spleen is a major
potential of the α2-agonists to activate the vagus nerve. Recent
studies, however, rule out a cholinergic anti-inflammatory source of inflammatory cytokines in experimental sepsis, as
mechanism based on a direct cholinergic interaction between the
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