NDP-MSH inhibits neutrophil migration through nicotinic and adrenergic receptors in experimental peritonitis

Jozi Figueiredo, Ana Elisa Ferreira, Rangel Leal Silva, Luis Ulloa, Paolo Grieco, Thiago Mattar Cunha, Sérgio Henrique Ferreira, Fernando De Queiróz Cunha, Alexandre Kanashiro

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Melanocortin is a potent anti-inflammatory molecule. However, little is known about the effect of melanocortin on acute inflammatory processes such as neutrophil migration. In the present study, we investigated the ability of [Nle4, D-Phe7]-melanocyte-stimulating hormone (NDP-MSH), a semisynthetic melanocortin compound, in the inhibition of neutrophil migration in carrageenin-induced peritonitis model. Herein, subcutaneous pretreatment with NDP-MSH decreased neutrophil trafficking in the peritoneal cavity in a dose-dependent manner. NDP-MSH inhibited vascular leakage, leukocyte rolling, and adhesion and reduced peritoneal macrophage inflammatory protein 2, but not TNF-alpha, IL-1beta, IL-10, and keratinocyte-derived chemokine production. In addition, the effect on neutrophil migration was reverted by the pretreatment with both propranolol (a nonselective beta-adrenergic antagonist) and mecamylamine (a nonselective nicotinic antagonist) but not by splenectomy surgery. Moreover, NDP-MSH intracerebroventricular administration inhibited neutrophil migration, indicating participation of the central nervous system. Our results propose that the NDP-MSH effect may be due to a spleen-independent neuro-immune pathway that efficiently regulates excessive neutrophil recruitment to tissues.

Original languageEnglish (US)
Pages (from-to)311-318
Number of pages8
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Issue number4
StatePublished - Apr 2013

All Science Journal Classification (ASJC) codes

  • Pharmacology


  • Adrenergic receptors
  • Anti-inflammatory cholinergic pathway
  • Melanocortin
  • Neuroimmunomodulation
  • Neutrophil migration
  • Nicotinic receptors

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