Abstract
The inflammatory reflex is a neurophysiological mechanism that regulates the immune system. The aim of this work was to investigate the effects of an alpha7 nicotinic agonist (anabasine) treatment on serum cytokines production and on IL-12 production of splenic dendritic cells (DC) in ovalbumin (OVA)-sensitized mice. First we evaluate serum cytokines production: mice received one single dose (i.p.) of saline or anabasine and 30 min latter were sensitized with OVA (50 μg/mouse, s.c.). After 24 h, half of them were euthanized and the others were euthanized 7 days after the sensitization and blood was collected. In another experiment mice were treated and sensitized as the same way; 7 days later, mice were euthanized and the spleens were harvested. Splenocytes were stained for CD11c and IAb, primed with 1 mg of OVA, and 6 h later cells were permebilized and stained for intracellular IL-12. 24 h after sensitization anabasine decreased TNF and MCP-1 in the serum ( p < 0.05). 7 days after sensitization anabasine increased IL-6 in the serum ( p < 0.05). Moreover, anabasine decreased intracellular IL-12. We showed that the alpha-7 nicotinic receptor stimulation has anti-inflammatory properties 24 h after the sensitization and therefore possibly has a Th2-skewing effect. Moreover, alpha-7 nicotinic receptor stimulation decreases IL-12 production by splenic DCs. These finds suggest that the alpha-7 nicotinic receptor stimulation changes the immune sensitization development and regulates adaptive immunity.
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