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Titolo:
SULFATIDE-INDUCED L-SELECTIN ACTIVATION GENERATES INTRACELLULAR OXYGEN RADICALS IN HUMAN NEUTROPHILS - MODULATION BY EXTRACELLULAR ADENOSINE
Autore:
BENGTSSON T; GRENEGARD M; OLSSON A; SJOGREN F; STENDAHL O; ZALAVARY S;
Indirizzi:
LINKOPING UNIV,FAC HLTH SCI,DEPT MED MICROBIOL S-58185 LINKOPING SWEDEN LINKOPING UNIV,FAC HLTH SCI,DEPT PHARMACOL S-58185 LINKOPING SWEDEN LINKOPING UNIV,FAC HLTH SCI,DEPT DERMATOL S-58185 LINKOPING SWEDEN
Titolo Testata:
Biochimica et biophysica acta. Molecular cell research
fascicolo: 2, volume: 1313, anno: 1996,
pagine: 119 - 129
SICI:
0167-4889(1996)1313:2<119:SLAGIO>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN POLYMORPHONUCLEAR LEUKOCYTES; SUPEROXIDE ANION GENERATION; CYTOSOLIC-FREE CALCIUM; TYROSINE PHOSPHORYLATION; CHEMOTACTIC FACTORS; CELL-ADHESION; BINDING-SITES; A2 RECEPTORS; INHIBITION; KINASE;
Keywords:
L-SELECTIN; SULFATIDE; OXYGEN RADICAL; NEUTROPHIL; ADENOSINE; TYROSINE PHOSPHORYLATION; CALCIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
T. Bengtsson et al., "SULFATIDE-INDUCED L-SELECTIN ACTIVATION GENERATES INTRACELLULAR OXYGEN RADICALS IN HUMAN NEUTROPHILS - MODULATION BY EXTRACELLULAR ADENOSINE", Biochimica et biophysica acta. Molecular cell research, 1313(2), 1996, pp. 119-129

Abstract

The sulfated form of galactocerebrosides (sulfatides) have recently been established as ligands for L-selectin. In this study we show that exposure of human neutrophils to sulfatides induces a transient generation of oxygen radicals, revealed by the luminol-enhanced chemiluminescence (CL) technique. The CL response was mainly located intracellularly, and was dependent on sulfation of the galactose ring, since non-sulfated galactocerebrosides had no effect. Sulfatides also dramaticallyamplified the CL response triggered by the chemotactic peptide formylmethionyl-leucyl-phenylalanine (fMLP). This effect was primarily due to an increased (up to 10-fold) intracellular generation of oxygen metabolites. Removal or blocking of L-selectin with chymotrypsin and monoclonal antibodies, respectively, markedly reduced the effects of sulfatides. Furthermore, sulfatides amplified the CL response triggered by ionomycin, whereas the response induced by phorbol-12-myristate-13-acetate was slightly reduced. The tyrosine kinase inhibitor, genistein, markedly inhibited the oxygen radical production induced by sulfatides, and totally abolished the potentiating effects of sulfatides in fMLP- and ionomycin-stimulated neutrophils. Sulfatides also triggered a transient rise in the intracellular free calcium concentration, [Ca2+](i). Consequently, L-selectin activation through sulfatides appear to affect oxidase activity through a Ca2+-dependent pathway involving tyrosine phosphorylation. Adenosine is an anti-inflammatory agent predominately released from the vascular endothelium which might suppress an inappropriate activation of the oxidase during L-selectin-mediated rollingof neutrophils. Indeed, we found that adenosine inhibited the oxidative burst induced by sulfatides, mainly by attenuating the intracellular generation of oxygen radicals. However, 10-100 times higher concentration of exogenous adenosine was required to inhibit the CL response induced by sulfatides to the same extent as the adenosine-mediated inhibition of the fMLP-induced response. This difference in sensitivity toadenosine could be explained by various expression of extracellular adenosine deaminase (ADA), since we found that the ADA-inhibitor erythro-9-(2-hydroxy-3-nonyl)-adenine (EHNA) markedly reduced the oxygen radical production caused by sulfatides and almost totally abolished the potentiating effects of sulfatides on the fMLP-induced respiratory burst. In contrary, EHNA only slightly reduced the fMLP-triggered CL response. We suggest that the initial activation of L-selectin prepare theneutrophil for an effective microbicidal activity in the extravascular space. This process might be dependent on a L-selectin-mediated increase in the expression and activity of ADA, which locally reduces the extracellular level of adenosine.

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Documento generato il 23/01/21 alle ore 09:04:32