Identification of novel peptides that stimulate human neutrophils

• Published in: Experimental & molecular medicine Vol. 44; no. 2; pp. 130 - 137
• Main Authors: Bae, Geon Ho, Lee, Ha Young, Jung, Young Su, Shim, Jae Woong, Kim, Sang Doo, Baek, Suk-Hwan, Kwon, Jae Young, Park, Joon Seong, Bae, Yoe-Sik
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 29.02.2012; Springer Nature B.V; Korean Society for Biochemistry and Molecular Biology; 생화학분자생물학회
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Calcium - metabolism; Cell Line; Cells, Cultured; Chemotaxis, Leukocyte - drug effects; Humans; Medical Biochemistry; Mice; Molecular Medicine; Neutrophils - cytology; Neutrophils - drug effects; NIH 3T3 Cells; Original; PC12 Cells; Peptides - pharmacology; Rats; Receptors, Formyl Peptide - agonists; Stem Cells; 생화학; peptides; calcium; receptors, formyl peptide; neutrophils; peptide library; chemotaxis
• ISSN: 1226-3613; 2092-6413
• DOI: 10.3858/emm.2012.44.2.008

Neutrophils play a key role in innate immunity, and the identification of new stimuli that stimulate neutrophil activity is a very important issue. In this study, we identified three novel peptides by screening a synthetic hexapeptide combinatorial library. The identified peptides GMMWAI, MMHWAM, and MMHWFM caused an increase in intracellular Ca 2+ in a concentration-dependent manner via phospholipase C activity in human neutrophils. The three peptides acted specifically on neutrophils and monocytes and not on other non-leukocytic cells. As a physiological characteristic of the peptides, we observed that the three peptides induced chemotactic migration of neutrophils as well as stimulated superoxide anion production. Studying receptor specificity, we observed that two of the peptides (GMMWAI and MMHWFM) acted on formyl peptide receptor (FPR)1 while the other peptide (MMHWAM) acted on FPR2. Since the three novel peptides were specific agonists for FPR1 or FPR2, they might be useful tools to study FPR1- or FPR2-mediated immune response and signaling.