Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation
Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its ant...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wu, Ben-Quan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer Basel AG 2011 |
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| Übergeordnetes Werk: |
Enthalten in: Inflammation research - Cham : Springer International Publishing AG, 1969, 60(2011), 8 vom: 19. Apr., Seite 775-782 |
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| Übergeordnetes Werk: |
volume:60 ; year:2011 ; number:8 ; day:19 ; month:04 ; pages:775-782 |
| Links: |
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| DOI / URN: |
10.1007/s00011-011-0333-6 |
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| Katalog-ID: |
SPR000015466 |
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| 245 | 1 | 0 | |a Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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| 520 | |a Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. | ||
| 650 | 4 | |a Lipoteichoic acid |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Platelet aggregation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a P-selectin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Soluble CD40L |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Platelet–monocyte aggregation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Zhi, Ming-Jun |4 aut | |
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| 700 | 1 | |a Huang, Jing |4 aut | |
| 700 | 1 | |a Zhou, Yu-Qi |4 aut | |
| 700 | 1 | |a Zhang, Tian-Tuo |4 aut | |
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10.1007/s00011-011-0333-6 doi (DE-627)SPR000015466 (SPR)s00011-011-0333-6-e DE-627 ger DE-627 rakwb eng Wu, Ben-Quan verfasserin aut Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Basel AG 2011 Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 Zhi, Ming-Jun aut Liu, Hui aut Huang, Jing aut Zhou, Yu-Qi aut Zhang, Tian-Tuo aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 60(2011), 8 vom: 19. Apr., Seite 775-782 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:60 year:2011 number:8 day:19 month:04 pages:775-782 https://dx.doi.org/10.1007/s00011-011-0333-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2011 8 19 04 775-782 |
| spelling |
10.1007/s00011-011-0333-6 doi (DE-627)SPR000015466 (SPR)s00011-011-0333-6-e DE-627 ger DE-627 rakwb eng Wu, Ben-Quan verfasserin aut Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Basel AG 2011 Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 Zhi, Ming-Jun aut Liu, Hui aut Huang, Jing aut Zhou, Yu-Qi aut Zhang, Tian-Tuo aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 60(2011), 8 vom: 19. Apr., Seite 775-782 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:60 year:2011 number:8 day:19 month:04 pages:775-782 https://dx.doi.org/10.1007/s00011-011-0333-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2011 8 19 04 775-782 |
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10.1007/s00011-011-0333-6 doi (DE-627)SPR000015466 (SPR)s00011-011-0333-6-e DE-627 ger DE-627 rakwb eng Wu, Ben-Quan verfasserin aut Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Basel AG 2011 Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 Zhi, Ming-Jun aut Liu, Hui aut Huang, Jing aut Zhou, Yu-Qi aut Zhang, Tian-Tuo aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 60(2011), 8 vom: 19. Apr., Seite 775-782 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:60 year:2011 number:8 day:19 month:04 pages:775-782 https://dx.doi.org/10.1007/s00011-011-0333-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2011 8 19 04 775-782 |
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10.1007/s00011-011-0333-6 doi (DE-627)SPR000015466 (SPR)s00011-011-0333-6-e DE-627 ger DE-627 rakwb eng Wu, Ben-Quan verfasserin aut Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Basel AG 2011 Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 Zhi, Ming-Jun aut Liu, Hui aut Huang, Jing aut Zhou, Yu-Qi aut Zhang, Tian-Tuo aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 60(2011), 8 vom: 19. Apr., Seite 775-782 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:60 year:2011 number:8 day:19 month:04 pages:775-782 https://dx.doi.org/10.1007/s00011-011-0333-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2011 8 19 04 775-782 |
| allfieldsSound |
10.1007/s00011-011-0333-6 doi (DE-627)SPR000015466 (SPR)s00011-011-0333-6-e DE-627 ger DE-627 rakwb eng Wu, Ben-Quan verfasserin aut Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Basel AG 2011 Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 Zhi, Ming-Jun aut Liu, Hui aut Huang, Jing aut Zhou, Yu-Qi aut Zhang, Tian-Tuo aut Enthalten in Inflammation research Cham : Springer International Publishing AG, 1969 60(2011), 8 vom: 19. Apr., Seite 775-782 (DE-627)253724031 (DE-600)1459194-7 1420-908X nnns volume:60 year:2011 number:8 day:19 month:04 pages:775-782 https://dx.doi.org/10.1007/s00011-011-0333-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 60 2011 8 19 04 775-782 |
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Enthalten in Inflammation research 60(2011), 8 vom: 19. Apr., Seite 775-782 volume:60 year:2011 number:8 day:19 month:04 pages:775-782 |
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Enthalten in Inflammation research 60(2011), 8 vom: 19. Apr., Seite 775-782 volume:60 year:2011 number:8 day:19 month:04 pages:775-782 |
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Lipoteichoic acid Platelet aggregation P-selectin Soluble CD40L Platelet–monocyte aggregation |
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Inflammation research |
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Wu, Ben-Quan @@aut@@ Zhi, Ming-Jun @@aut@@ Liu, Hui @@aut@@ Huang, Jing @@aut@@ Zhou, Yu-Qi @@aut@@ Zhang, Tian-Tuo @@aut@@ |
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2011-04-19T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR000015466</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519235934.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201001s2011 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00011-011-0333-6</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR000015466</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00011-011-0333-6-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Wu, Ben-Quan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2011</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Springer Basel AG 2011</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. 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|
| author |
Wu, Ben-Quan |
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Wu, Ben-Quan misc Lipoteichoic acid misc Platelet aggregation misc P-selectin misc Soluble CD40L misc Platelet–monocyte aggregation Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation Lipoteichoic acid (dpeaa)DE-He213 Platelet aggregation (dpeaa)DE-He213 P-selectin (dpeaa)DE-He213 Soluble CD40L (dpeaa)DE-He213 Platelet–monocyte aggregation (dpeaa)DE-He213 |
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misc Lipoteichoic acid misc Platelet aggregation misc P-selectin misc Soluble CD40L misc Platelet–monocyte aggregation |
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misc Lipoteichoic acid misc Platelet aggregation misc P-selectin misc Soluble CD40L misc Platelet–monocyte aggregation |
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Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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Wu, Ben-Quan |
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Inflammation research |
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Wu, Ben-Quan Zhi, Ming-Jun Liu, Hui Huang, Jing Zhou, Yu-Qi Zhang, Tian-Tuo |
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Wu, Ben-Quan |
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inhibitory effects of lipoteichoic acid from staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
| abstract |
Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. © Springer Basel AG 2011 |
| abstractGer |
Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. © Springer Basel AG 2011 |
| abstract_unstemmed |
Objective Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet–monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet–monocyte aggregation. Methods Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2 weeks. Washed platelets were prepared and incubated with LTA (0.5–2.0 μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet–monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. Results LTA dose-dependently decreased platelet aggregation from 89.32 ± 10.24% to 36.28 ± 9.01% (P < 0.05), sCD40L release from 3.28 ± 0.76 to 1.13 ± 0.45 ng/mL (P < 0.05) and surface P-selectin expression from 82.01 ± 11.20 to 22.78 ± 6.42% (P < 0.05). In human whole blood, 1.0 μg/mL LTA inhibited platelet–monocyte aggregation from 78.19 ± 10.94 to 38.24 + 8.74% (P < 0.05). Conclusions These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet–monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus. © Springer Basel AG 2011 |
| collection_details |
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| title_short |
Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation |
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https://dx.doi.org/10.1007/s00011-011-0333-6 |
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Zhi, Ming-Jun Liu, Hui Huang, Jing Zhou, Yu-Qi Zhang, Tian-Tuo |
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Zhi, Ming-Jun Liu, Hui Huang, Jing Zhou, Yu-Qi Zhang, Tian-Tuo |
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10.1007/s00011-011-0333-6 |
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2024-07-03T13:28:51.014Z |
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| score |
7.402935 |