Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection

To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Helene Möllerherm [verfasserIn] Katja Branitzki-Heinemann [verfasserIn] Graham Brogden [verfasserIn] Ayssar A. Elamin [verfasserIn] Wulf Oehlmann [verfasserIn] Herbert Fuhrmann [verfasserIn] Mahavir Singh [verfasserIn] Hassan Y. Naim [verfasserIn] Maren von Köckritz-Blickwede [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α

Übergeordnetes Werk:	In: Frontiers in Immunology - Frontiers Media S.A., 2011, 8(2017)
Übergeordnetes Werk:	volume:8 ; year:2017

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fimmu.2017.00541

Katalog-ID:	DOAJ042400805

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allfields	10.3389/fimmu.2017.00541 doi (DE-627)DOAJ042400805 (DE-599)DOAJ7c2c476cf1dc4e4f829d320409cc76cd DE-627 ger DE-627 rakwb eng RC581-607 Helene Möllerherm verfasserin aut Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy Katja Branitzki-Heinemann verfasserin aut Graham Brogden verfasserin aut Ayssar A. Elamin verfasserin aut Wulf Oehlmann verfasserin aut Herbert Fuhrmann verfasserin aut Mahavir Singh verfasserin aut Hassan Y. Naim verfasserin aut Maren von Köckritz-Blickwede verfasserin aut Maren von Köckritz-Blickwede verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 8(2017) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:8 year:2017 https://doi.org/10.3389/fimmu.2017.00541 kostenfrei https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd kostenfrei http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_2003 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 8 2017
spelling	10.3389/fimmu.2017.00541 doi (DE-627)DOAJ042400805 (DE-599)DOAJ7c2c476cf1dc4e4f829d320409cc76cd DE-627 ger DE-627 rakwb eng RC581-607 Helene Möllerherm verfasserin aut Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy Katja Branitzki-Heinemann verfasserin aut Graham Brogden verfasserin aut Ayssar A. Elamin verfasserin aut Wulf Oehlmann verfasserin aut Herbert Fuhrmann verfasserin aut Mahavir Singh verfasserin aut Hassan Y. Naim verfasserin aut Maren von Köckritz-Blickwede verfasserin aut Maren von Köckritz-Blickwede verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 8(2017) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:8 year:2017 https://doi.org/10.3389/fimmu.2017.00541 kostenfrei https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd kostenfrei http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_2003 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 8 2017
allfields_unstemmed	10.3389/fimmu.2017.00541 doi (DE-627)DOAJ042400805 (DE-599)DOAJ7c2c476cf1dc4e4f829d320409cc76cd DE-627 ger DE-627 rakwb eng RC581-607 Helene Möllerherm verfasserin aut Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy Katja Branitzki-Heinemann verfasserin aut Graham Brogden verfasserin aut Ayssar A. Elamin verfasserin aut Wulf Oehlmann verfasserin aut Herbert Fuhrmann verfasserin aut Mahavir Singh verfasserin aut Hassan Y. Naim verfasserin aut Maren von Köckritz-Blickwede verfasserin aut Maren von Köckritz-Blickwede verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 8(2017) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:8 year:2017 https://doi.org/10.3389/fimmu.2017.00541 kostenfrei https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd kostenfrei http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_2003 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 8 2017
allfieldsGer	10.3389/fimmu.2017.00541 doi (DE-627)DOAJ042400805 (DE-599)DOAJ7c2c476cf1dc4e4f829d320409cc76cd DE-627 ger DE-627 rakwb eng RC581-607 Helene Möllerherm verfasserin aut Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy Katja Branitzki-Heinemann verfasserin aut Graham Brogden verfasserin aut Ayssar A. Elamin verfasserin aut Wulf Oehlmann verfasserin aut Herbert Fuhrmann verfasserin aut Mahavir Singh verfasserin aut Hassan Y. Naim verfasserin aut Maren von Köckritz-Blickwede verfasserin aut Maren von Köckritz-Blickwede verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 8(2017) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:8 year:2017 https://doi.org/10.3389/fimmu.2017.00541 kostenfrei https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd kostenfrei http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_2003 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 8 2017
allfieldsSound	10.3389/fimmu.2017.00541 doi (DE-627)DOAJ042400805 (DE-599)DOAJ7c2c476cf1dc4e4f829d320409cc76cd DE-627 ger DE-627 rakwb eng RC581-607 Helene Möllerherm verfasserin aut Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage. mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy Katja Branitzki-Heinemann verfasserin aut Graham Brogden verfasserin aut Ayssar A. Elamin verfasserin aut Wulf Oehlmann verfasserin aut Herbert Fuhrmann verfasserin aut Mahavir Singh verfasserin aut Hassan Y. Naim verfasserin aut Maren von Köckritz-Blickwede verfasserin aut Maren von Köckritz-Blickwede verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 8(2017) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:8 year:2017 https://doi.org/10.3389/fimmu.2017.00541 kostenfrei https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd kostenfrei http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 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_2003 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 8 2017
language	English
source	In Frontiers in Immunology 8(2017) volume:8 year:2017
sourceStr	In Frontiers in Immunology 8(2017) volume:8 year:2017
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α Immunologic diseases. Allergy
isfreeaccess_bool	true
container_title	Frontiers in Immunology
authorswithroles_txt_mv	Helene Möllerherm @@aut@@ Katja Branitzki-Heinemann @@aut@@ Graham Brogden @@aut@@ Ayssar A. Elamin @@aut@@ Wulf Oehlmann @@aut@@ Herbert Fuhrmann @@aut@@ Mahavir Singh @@aut@@ Hassan Y. Naim @@aut@@ Maren von Köckritz-Blickwede @@aut@@
publishDateDaySort_date	2017-01-01T00:00:00Z
hierarchy_top_id	657998354
id	DOAJ042400805
language_de	englisch
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callnumber-first	R - Medicine
author	Helene Möllerherm
spellingShingle	Helene Möllerherm misc RC581-607 misc mast cells misc innate immunity misc extracellular traps misc degranulation misc hypoxia misc hypoxia-inducible factor 1α misc Immunologic diseases. Allergy Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection
authorStr	Helene Möllerherm
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topic_title	RC581-607 Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection mast cells innate immunity extracellular traps degranulation hypoxia hypoxia-inducible factor 1α
topic	misc RC581-607 misc mast cells misc innate immunity misc extracellular traps misc degranulation misc hypoxia misc hypoxia-inducible factor 1α misc Immunologic diseases. Allergy
topic_unstemmed	misc RC581-607 misc mast cells misc innate immunity misc extracellular traps misc degranulation misc hypoxia misc hypoxia-inducible factor 1α misc Immunologic diseases. Allergy
topic_browse	misc RC581-607 misc mast cells misc innate immunity misc extracellular traps misc degranulation misc hypoxia misc hypoxia-inducible factor 1α misc Immunologic diseases. Allergy
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title	Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection
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title_full	Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection
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author_browse	Helene Möllerherm Katja Branitzki-Heinemann Graham Brogden Ayssar A. Elamin Wulf Oehlmann Herbert Fuhrmann Mahavir Singh Hassan Y. Naim Maren von Köckritz-Blickwede
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title_sort	hypoxia modulates the response of mast cells to staphylococcus aureus infection
callnumber	RC581-607
title_auth	Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection
abstract	To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage.
abstractGer	To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage.
abstract_unstemmed	To study the antimicrobial function of immune cells ex vivo, cells are commonly cultivated under atmospheric oxygen concentrations (20–21%; normoxia), although the physiological oxygen conditions in vivo are significantly lower in most tissues. Especially during an acute infection, oxygen concentration locally decreases to hypoxic levels around or below 1%. The goal of this study was to investigate the effect of hypoxia on the activity of mast cells (MCs). MCs were cultivated for 3 or 24 h at 1% O2 in a hypoxia glove box and co-incubated with heat-inactivated Staphylococcus aureus. When incubating the cells for 24 h under hypoxia, the transcriptional regulator hypoxia-inducible factor 1α (HIF-1α) was stabilized and resulted in increased extracellular trap formation and decreased phagocytosis. Interestingly, while phagocytosis of fluorescent S. aureus bioparticles as well as the release of extracellular traps remained unaffected at 3 h hypoxia, the secretion of the prestored mediator histamine was increased under hypoxia alone. In contrast, the release of TNF-α was generally reduced at 3 h hypoxia. Microarray transcriptome analysis revealed 13 genes that were significantly downregulated in MCs comparing 3 h hypoxia versus normoxia. One interesting candidate is sec24, a member of the pre-budding complex of coat protein complex II (COPII), which is responsible for the anterograde transport of proteins from the ER to the Golgi apparatus. These data lead to the suggestion that de novo synthesized proteins including crucial factors, which are involved in the response to an acute infection like TNF-α, may eventually be retained in the ER under hypoxia. Importantly, the expression of HIF-1α was not altered at 3 h. Thus, our data exhibit a HIF-1α-independent reaction of MCs to short-term hypoxia. We hypothesize that MCs respond to short-term low oxygen levels in a HIF-1α-independent manner by downregulating the release of proinflammatory cytokines like TNF-α, thereby avoiding uncontrolled degranulation, which could lead to excessive inflammation and severe tissue damage.
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title_short	Hypoxia Modulates the Response of Mast Cells to Staphylococcus aureus Infection
url	https://doi.org/10.3389/fimmu.2017.00541 https://doaj.org/article/7c2c476cf1dc4e4f829d320409cc76cd http://journal.frontiersin.org/article/10.3389/fimmu.2017.00541/full https://doaj.org/toc/1664-3224
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author2	Katja Branitzki-Heinemann Graham Brogden Ayssar A. Elamin Wulf Oehlmann Herbert Fuhrmann Mahavir Singh Hassan Y. Naim Maren von Köckritz-Blickwede
author2Str	Katja Branitzki-Heinemann Graham Brogden Ayssar A. Elamin Wulf Oehlmann Herbert Fuhrmann Mahavir Singh Hassan Y. Naim Maren von Köckritz-Blickwede
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up_date	2024-07-04T00:49:31.389Z
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