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Changes in the ratio between FPR and FPRL1 triggered superoxide production in human neutrophils-a tool in analysing receptor specific events

Artikel i vetenskaplig tidskrift
Författare Huamei Fu
Jennie Karlsson
Lena Björkman
Anna-Lena Stenfeldt
Anna Karlsson
Johan Bylund
Claes Dahlgren
Publicerad i Journal of Immunological Methods
Volym 331
Nummer/häfte 1-2
Sidor 50-8
ISSN 0022-1759
Publiceringsår 2008
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 50-8
Språk en
Länkar dx.doi.org/10.1016/j.jim.2007.11.00...
Ämnesord Cyclooxygenase Inhibitors/pharmacology, HL-60 Cells, Humans, Neutrophils/drug effects/immunology/*metabolism, Oligopeptides/immunology/pharmacology, Piroxicam/pharmacology, Receptors, Formyl Peptide/agonists/immunology/*metabolism, Receptors, Lipoxin/agonists/immunology/*metabolism, Sodium Dodecyl Sulfate/pharmacology, Superoxides/*metabolism
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Neutrophils express the G protein-coupled N-formyl peptide receptor (FPR) as well as its closely related homologue, formyl peptide like receptor 1 (FPRL1), and activation of these receptors induce a release of superoxide anions. The magnitude of the responses induced by the two peptide agonists fMLF and WKYMVM, specific for FPR and FPRL1, respectively, was found to be very variable in different neutrophil populations. The ratio between the FPR and FPRL1 triggered respiratory burst was, however, very constant and close to 1. The ratio was changed in neutrophils that were desensitized as well as when the signaling through either of the receptors was inhibited by receptor specific antagonists or by a PIP(2) binding peptide. The FPR/FPRL1 ratio was not changed in primed neutrophils or in differentiated HL-60 cells. We show that the change in the ratio, calculated from the amount of radical release in neutrophils triggered with FPR and FPRL1 specific agonists can be used as a valuable tool to find/identify receptor specific/selective changes mediated by peptides/proteins/drugs, as well as to identify cells from patients or groups of patients that diverge from normal cells in their FPR/FPRL1 triggered functions.

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