Journal
INFLAMMATION
Volume 39, Issue 4, Pages 1405-1413Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-016-0372-9
Keywords
isoproterenol; neutrophil; neuroimmunomodulation; beta-adrenergic receptor; nicotinic receptor
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Funding
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [11/20343-4, 11/19670-0, 12/04237-2, 13/01466-3, 13/08216-2]
- National Council for Scientific and Technological Development (CNPq) [142068/2012-8]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [451/2008]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [13/01466-3, 13/08216-2, 12/04237-2] Funding Source: FAPESP
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The aim of this study was to identify the effect of beta-adrenergic receptor activation on neutrophil migration in experimental peritonitis elucidating the neuroimmune components involved such as nicotinic receptors and the spleen. Mice pre-treated with mecamylamine (nicotinic antagonist) and propranolol (beta-adrenergic antagonist) or splenectomized animals were treated with isoproterenol (beta-adrenergic agonist) prior to intraperitoneal injection of carrageenan. After 4 h, the infiltrating neutrophils and the local cytokine/chemokine levels were evaluated in the peritoneal lavage. The effect of isoproterenol on neutrophil chemotaxis was investigated in a Boyden chamber. Isoproterenol inhibited neutrophil trafficking, reducing the cytokine/chemokine release and neutrophil chemotaxis. Surprisingly, the isoproterenol effect on neutrophil migration was totally reverted by splenectomy and mecamylamine pre-treatment. In contrast, the inhibitory effect of nicotine on neutrophil migration was abrogated only by splenectomy but not by propranolol pre-treatment. Collectively, our data show that beta-adrenergic receptor activation regulates the acute neutrophil recruitment via splenic nicotinic receptor.
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