The role of neutrophils in immune dysfunction during severe inflammation
Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune par...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Leliefeld, Pieter H. C. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016 |
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| Schlagwörter: |
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| Anmerkung: |
© Leliefeld et al. 2016 |
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| Übergeordnetes Werk: |
Enthalten in: Critical care - London : BioMed Central, 1997, 20(2016), 1 vom: 23. März |
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| Übergeordnetes Werk: |
volume:20 ; year:2016 ; number:1 ; day:23 ; month:03 |
| Links: |
|---|
| DOI / URN: |
10.1186/s13054-016-1250-4 |
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SPR029893232 |
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| 245 | 1 | 4 | |a The role of neutrophils in immune dysfunction during severe inflammation |
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| 520 | |a Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. | ||
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| 700 | 1 | |a Pillay, Janesh |4 aut | |
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10.1186/s13054-016-1250-4 doi (DE-627)SPR029893232 (SPR)s13054-016-1250-4-e DE-627 ger DE-627 rakwb eng Leliefeld, Pieter H. C. verfasserin aut The role of neutrophils in immune dysfunction during severe inflammation 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Leliefeld et al. 2016 Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. Chronic Granulomatous Disease (dpeaa)DE-He213 Neutrophil Elastase (dpeaa)DE-He213 Severe Inflammation (dpeaa)DE-He213 Neutrophil Extracellular Trap (dpeaa)DE-He213 Chronic Granulomatous Disease Patient (dpeaa)DE-He213 Wessels, Catharina M. aut Leenen, Luke P. H. aut Koenderman, Leo aut Pillay, Janesh aut Enthalten in Critical care London : BioMed Central, 1997 20(2016), 1 vom: 23. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:20 year:2016 number:1 day:23 month:03 https://dx.doi.org/10.1186/s13054-016-1250-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2016 1 23 03 |
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10.1186/s13054-016-1250-4 doi (DE-627)SPR029893232 (SPR)s13054-016-1250-4-e DE-627 ger DE-627 rakwb eng Leliefeld, Pieter H. C. verfasserin aut The role of neutrophils in immune dysfunction during severe inflammation 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Leliefeld et al. 2016 Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. Chronic Granulomatous Disease (dpeaa)DE-He213 Neutrophil Elastase (dpeaa)DE-He213 Severe Inflammation (dpeaa)DE-He213 Neutrophil Extracellular Trap (dpeaa)DE-He213 Chronic Granulomatous Disease Patient (dpeaa)DE-He213 Wessels, Catharina M. aut Leenen, Luke P. H. aut Koenderman, Leo aut Pillay, Janesh aut Enthalten in Critical care London : BioMed Central, 1997 20(2016), 1 vom: 23. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:20 year:2016 number:1 day:23 month:03 https://dx.doi.org/10.1186/s13054-016-1250-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2016 1 23 03 |
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10.1186/s13054-016-1250-4 doi (DE-627)SPR029893232 (SPR)s13054-016-1250-4-e DE-627 ger DE-627 rakwb eng Leliefeld, Pieter H. C. verfasserin aut The role of neutrophils in immune dysfunction during severe inflammation 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Leliefeld et al. 2016 Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. Chronic Granulomatous Disease (dpeaa)DE-He213 Neutrophil Elastase (dpeaa)DE-He213 Severe Inflammation (dpeaa)DE-He213 Neutrophil Extracellular Trap (dpeaa)DE-He213 Chronic Granulomatous Disease Patient (dpeaa)DE-He213 Wessels, Catharina M. aut Leenen, Luke P. H. aut Koenderman, Leo aut Pillay, Janesh aut Enthalten in Critical care London : BioMed Central, 1997 20(2016), 1 vom: 23. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:20 year:2016 number:1 day:23 month:03 https://dx.doi.org/10.1186/s13054-016-1250-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2016 1 23 03 |
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10.1186/s13054-016-1250-4 doi (DE-627)SPR029893232 (SPR)s13054-016-1250-4-e DE-627 ger DE-627 rakwb eng Leliefeld, Pieter H. C. verfasserin aut The role of neutrophils in immune dysfunction during severe inflammation 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Leliefeld et al. 2016 Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. Chronic Granulomatous Disease (dpeaa)DE-He213 Neutrophil Elastase (dpeaa)DE-He213 Severe Inflammation (dpeaa)DE-He213 Neutrophil Extracellular Trap (dpeaa)DE-He213 Chronic Granulomatous Disease Patient (dpeaa)DE-He213 Wessels, Catharina M. aut Leenen, Luke P. H. aut Koenderman, Leo aut Pillay, Janesh aut Enthalten in Critical care London : BioMed Central, 1997 20(2016), 1 vom: 23. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:20 year:2016 number:1 day:23 month:03 https://dx.doi.org/10.1186/s13054-016-1250-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2016 1 23 03 |
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10.1186/s13054-016-1250-4 doi (DE-627)SPR029893232 (SPR)s13054-016-1250-4-e DE-627 ger DE-627 rakwb eng Leliefeld, Pieter H. C. verfasserin aut The role of neutrophils in immune dysfunction during severe inflammation 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Leliefeld et al. 2016 Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. Chronic Granulomatous Disease (dpeaa)DE-He213 Neutrophil Elastase (dpeaa)DE-He213 Severe Inflammation (dpeaa)DE-He213 Neutrophil Extracellular Trap (dpeaa)DE-He213 Chronic Granulomatous Disease Patient (dpeaa)DE-He213 Wessels, Catharina M. aut Leenen, Luke P. H. aut Koenderman, Leo aut Pillay, Janesh aut Enthalten in Critical care London : BioMed Central, 1997 20(2016), 1 vom: 23. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:20 year:2016 number:1 day:23 month:03 https://dx.doi.org/10.1186/s13054-016-1250-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2016 1 23 03 |
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Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. © Leliefeld et al. 2016 |
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Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. © Leliefeld et al. 2016 |
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Abstract Critically ill post-surgical, post-trauma and/or septic patients are characterised by severe inflammation. This immune response consists of both a pro- and an anti-inflammatory component. The pro-inflammatory component contributes to (multiple) organ failure whereas occurrence of immune paralysis predisposes to infections. Strikingly, infectious complications arise in these patients despite the presence of a clear neutrophilia. We propose that dysfunction of neutrophils potentially increases the susceptibility to infections or can result in the inability to clear existing infections. Under homeostatic conditions these effector cells of the innate immune system circulate in a quiescent state and serve as the first line of defence against invading pathogens. In severe inflammation, however, neutrophils are rapidly activated, which affects their functional capacities, such as chemotaxis, phagocytosis, intra-cellular killing, NETosis, and their capacity to modulate adaptive immunity. This review provides an overview of the current understanding of neutrophil dysfunction in severe inflammation. We will discuss the possible mechanisms of downregulation of anti-microbial function, suppression of adaptive immunity by neutrophils and the contribution of neutrophil subsets to immune paralysis. © Leliefeld et al. 2016 |
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| score |
7.4004955 |