The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease
HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and it...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gauthier, Alex [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:120 ; year:2018 ; day:20 ; month:05 ; pages:88 |
| Links: |
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| DOI / URN: |
10.1016/j.freeradbiomed.2018.04.291 |
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| 520 | |a HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. | ||
| 520 | |a HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. | ||
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10.1016/j.freeradbiomed.2018.04.291 doi GBV00000000000233A.pica (DE-627)ELV043056881 (ELSEVIER)S0891-5849(18)30456-8 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. Sitapara, Ravi oth Wang, Mao oth Antoine, Dan oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.291 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.291 doi GBV00000000000233A.pica (DE-627)ELV043056881 (ELSEVIER)S0891-5849(18)30456-8 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. Sitapara, Ravi oth Wang, Mao oth Antoine, Dan oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.291 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.291 doi GBV00000000000233A.pica (DE-627)ELV043056881 (ELSEVIER)S0891-5849(18)30456-8 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. Sitapara, Ravi oth Wang, Mao oth Antoine, Dan oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.291 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.291 doi GBV00000000000233A.pica (DE-627)ELV043056881 (ELSEVIER)S0891-5849(18)30456-8 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. Sitapara, Ravi oth Wang, Mao oth Antoine, Dan oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.291 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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10.1016/j.freeradbiomed.2018.04.291 doi GBV00000000000233A.pica (DE-627)ELV043056881 (ELSEVIER)S0891-5849(18)30456-8 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Gauthier, Alex verfasserin aut The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease 2018transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. Sitapara, Ravi oth Wang, Mao oth Antoine, Dan oth Mantell, Lin oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:120 year:2018 day:20 month:05 pages:88 https://doi.org/10.1016/j.freeradbiomed.2018.04.291 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 120 2018 20 0520 88 120.2018, S88- 045F 570 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:120 year:2018 day:20 month:05 pages:88 |
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New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |
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The redox regulation of damage-associated molecular pattern molecule HMGB1 in pulmonary disease |
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HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. |
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HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. |
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HMGB1 is an endogenous molecule that can initiate and perpetuate inflammation. Previously, we have shown that airway HMGB1 mediates hyperoxia-induced acute lung injury and compromised innate immunity in cystic fibrosis and ventilator-associated pneumonia. To determine the redox state of HMGB1 and its effects on acute lung injury and innate immunity under hyperoxic conditions, LC-MS/MS was used to analyze HMGB1 in either bronchoalveolar lavage fluid (BAL) of mice or media of cultured macrophages exposed to 95–99% O2. MS/MS analysis indicated nuclear HMGB1 in both 95% and 21% O2 groups was in its reduced form, but in BAL or culture media, all three critical redox forms of HMGB1 were present. Extracellular HMGB1 was not detected in BAL or cultured macrophages that remained at 21% O2. GTS -21, a drug which can improve macrophage functions and alleviate hyperoxia-induced acute lung injury, kept extracellular HMGB1 in the reduced form. These data suggest that hyperoxia-induced oxidative modifications of HMGB1 occurred after its release into the airways. Strategies to prevent HMGB1 from oxidation may provide an effective approach to treat patients on ventilation with either lung injury and/or compromised host defense against bacterial infections. |
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