Staphylococcal serine proteinase increases intracellular free calcium concentration in human polymorphonuclear leukocytes

• Published in: Antonie van Leeuwenhoek 1997-10, Vol.72 (3), p.245-249
• Main Authors: NOWAK, D, KROL, M, MIEDZOBRODZKI, J, BIALASIEWICZ, P
• Format: Article
• Language: English
• Subjects: Adult; Bacterial Proteins - pharmacology; Bacteriology; Biological and medical sciences; Calcium; Calcium - metabolism; Calcium-Transporting ATPases - antagonists & inhibitors; Cell Compartmentation; Cells; Cells, Cultured; Chemotaxis, Leukocyte - drug effects; Enzyme Inhibitors - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Humans; Indoles - pharmacology; Intracellular Fluid - drug effects; Intracellular Fluid - metabolism; Ion Transport - drug effects; Male; Microbiology; N-Formylmethionine Leucyl-Phenylalanine - pharmacology; Neutrophils - drug effects; Neutrophils - metabolism; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Proteinase inhibitors; Serine Endopeptidases - pharmacology; Signal transduction
• ISSN: 0003-6072; 1572-9699
• DOI: 10.1023/A:1000478308243

Staphylococcal serine proteinase (SSP) can influence various functions of human polymorphonuclear leukocytes (PMNL) including chemotaxis and phagocytosis. Since the rise in intracellular free calcium concentration is an important step in signal transduction leading to phagocyte activation, we tested the ability of SSP to increase the intracellular free calcium concentration in human PMNL using the fluorescent calcium indicator Fura-2AM. PMNL isolated from healthy donors responded to SSP in the concentration range of 10 to 100 micrograms/ml. The highest Ca2+ rise (104 +/- 47 nM) was observed for 10 micrograms/ml SSP. It was mainly dependent (81 +/- 11%) on extracellular calcium influx, however, SSP mobilized 68 +/- 7% of Ca2+ from intracellular calcium stores. Boiling of SSP or preincubation with phenylmethylsulphonylfluoride (an serine proteinase inhibitor) did not change its ability to increase intracellular free calcium concentration in PMNL. It suggests that active center of SSP is not responsible for Ca2+ mobilization. Finally, PMNL responded to each of three consecutive stimulations with SSP independently of the presence of high or low extracellular Ca2+ concentration. This may be an additional mechanism responsible for activation of human PMNL and degradation of alveolar walls during the staphylococcal infection in the lower airways.