Priming of normal human neutrophils by tachykinins: tuftsin-like inhibition of in vitro chemotaxis stimulated by formylpeptide or interleukin-8
| Autor: | Christian J. Wiedermann, Dietmar Geissler, Ivan Lindley, Monika Niedermühlbichler, U Zilian, Herbert Braunsteiner |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
medicine.medical_specialty
Phagocyte Neutrophils Physiology medicine.drug_class Molecular Sequence Data Clinical Biochemistry Tuftsin Substance P In Vitro Techniques Biology Pharmacology Biochemistry Cellular and Molecular Neuroscience chemistry.chemical_compound Endocrinology Tachykinins Internal medicine medicine Humans Amino Acid Sequence Interleukin 8 Chemotactic Factors Interleukin-8 Chemotaxis Receptor antagonist Chemotaxis Leukocyte medicine.anatomical_structure chemistry Tumor necrosis factor alpha Neurokinin A |
| Zdroj: | Regulatory Peptides. 36:359-368 |
| ISSN: | 0167-0115 |
| DOI: | 10.1016/0167-0115(91)90069-s |
| Popis: | Tachykinins have priming effects on polymorphonuclear neutrophils, since they may activate the neutrophils to exhibit an exaggerated inflammatory response to phlogistic mediators. In order to investigate mechanisms involved in this action, we determined the influence of substance P and neurokinin A on chemotaxis of human neutrophils towards gradients of formymethionyl-leucyl-phenylalanine or recombinant human interleukin-8. As seen with other neutrophil-priming agents such as tumor necrosis factor-α, exposure of neutrophils to substance P or neurokinin A had an inhibitory effect upon a stimulated migration, with effective concentrations being in the nanomolar range. Tuftsin, a known neutrophil activating peptide, similarly inhibited stimulated migration. Analysis of structure-activity relationships revealed that activity of tachykinins is located in amino-terminal, tuftsin-like sequences. The inhibition of stimulated migration was partly reversed by (Pro 1 )-tuftsin, a partial tuftsin receptor antagonist, which suggests that the effect of amino-terminal tachykinins involves activation of tuftsin receptors of neutrophils. |
| Databáze: | OpenAIRE |
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