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(Journal of Leukocyte Biology. 2001;69:1013-1018.)
© 2001 by Society for Leukocyte Biology

Priming effects of substance P on calcium changes evoked by interleukin-8 in human neutrophils

Chiara Dianzani^*, Grazia Lombardi, Massimo Collino^*, Cinzia Ferrara, Maria Chiara Cassone^* and Roberto Fantozzi^*

^* Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Turin, Italy, and
Department of Alimentary, Chemical, Pharmaceutical and Pharmacological Sciences, University of Piemonte Orientale, Novara, Italy

Correspondence: Roberto Fantozzi, Dipartimento di Anatomia, Farmacologia e Medicina Legale, Università di Torino, Via Pietro Giuria 9, 10125 Torino, Italy. E-mail: roberto.fantozzi{at}unito.it

The neurokinin (NK) substance P (SP), which is a mediator of neurogenic inflammation, has been reported to prime human polymorphonuclear neutrophils (PMNs). The priming effects of SP on PMNs activated by recombinant interleukin-8 (rIL-8) were investigated. SP enhanced, in a dose- and time-dependent way, the rise in cytosolic free-calcium concentration, [Ca²⁺]_i, evoked by the chemokine. The priming effects of SP were abolished by exposing PMNs to a calcium-free medium supplemented with EGTA. The C-terminal peptides SP(4–11) and SP(6–11) but not the N-terminal peptide SP(1–7) shared the priming effects of SP. The selective NK-1 receptor agonist [Sar-9, Met(O)₂-11]SP mimicked the effects of SP, which were not reproduced by the selective NK-2 receptor agonist [ßAla-8]-NKA(4–10) or the selective NK-3 agonist senktide. Two selective NK-1 antagonists, CP96,345 and L703,606, dose dependently inhibited SP priming effects. These results demonstrated that SP primes PMNs exposed to rIL-8 and suggested that SP priming effects are receptor mediated.

Key Words: cytosolic free-calcium concentration • neuropeptide • NK-1 receptor

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