Trp-Lys-Tyr-Met-Val-D-Met stimulates superoxide generation and killing of Staphylococcus aureus via phospholipase D activation in human monocytes
SCIE
SCOPUS
- Title
- Trp-Lys-Tyr-Met-Val-D-Met stimulates superoxide generation and killing of Staphylococcus aureus via phospholipase D activation in human monocytes
- Authors
- Bae, YS; Ju, SA; Kim, JY; Seo, JK; Baek, SH; Kwak, JY; Kim, BS; Suh, PG; Ryu, SH
- Date Issued
- 1999-02
- Publisher
- FEDERATION AMER SOC EXP BIOL
- Abstract
- Among the phagocytic leukocytes, monocytes have the important role of clearing out parasitic microorganisms, They accomplish this through production of toxic metabolites of oxygen, Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), a peptide that stimulates phosphoinositide (PI) hydrolysis in human leukocytes, including monocytes, binds to a unique cell surface receptor and stimulates superoxide generation, killing of Staphylococcus aureus, and activation of phospholipase D (PLD) in human monocytes. Preincubation of the cells with a PI-specific phospholipase C (PLC) inhibitor (U-73122), protein kinase C inhibitor (GF109203X), or intracellular Ca2+ chelator (BAPTA/AM) before the peptide stimulus totally inhibits the peptide-induced PLD activation and superoxide generation. On the other baud, tyrosine kinase inhibitor genistein only partially inhibits the peptide-induced processes, The peptide-induced bacteria killing activity shares regulatory mechanisms for PLD activation with the superoxide generation, which is inhibited in the presence of l-butanol, We suggest that the peptide stimulates PLD downstream of PLC activation and PLD activation in turn is essential for the peptide-induced immunological functions such as the superoxide generation and killing of bacteria by human monocytes.
- Keywords
- signal transduction; immunomodulators; lipid mediators; PROTEIN-KINASE-C; HUMAN NEUTROPHILS; RESPIRATORY BURST; PHOSPHOINOSITIDE HYDROLYSIS; PHOSPHATIDIC-ACID; PLASMA-MEMBRANE; NADPH OXIDASE; HL-60 CELLS; RECEPTOR; MECHANISMS
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/20512
- DOI
- 10.1002/jlb.65.2.241
- ISSN
- 0741-5400
- Article Type
- Article
- Citation
- JOURNAL OF LEUKOCYTE BIOLOGY, vol. 65, no. 2, page. 241 - 248, 1999-02
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