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Priming effects of substance P on calcium changes evoked by interleukin‐8 in human neutrophils
Author(s) -
Dianzani Chiara,
Lombardi Grazia,
Collino Massimo,
Ferrara Cinzia,
Cassone Maria Chiara,
Fantozzi Roberto
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.69.6.1013
Subject(s) - substance p , egta , agonist , priming (agriculture) , biology , receptor , medicine , endocrinology , neurokinin a , calcium , pharmacology , biochemistry , neuropeptide , botany , germination
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, [Ca 2+ ] 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 [βAla‐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.