Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP
Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the sub...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gustavo Rico-Llanos [verfasserIn] Óscar Porras-Perales [verfasserIn] Sandra Escalante [verfasserIn] Daniel B. Vázquez-Calero [verfasserIn] Lucía Valiente [verfasserIn] María I. Castillo [verfasserIn] José Miguel Pérez-Tejeiro [verfasserIn] David Baglietto-Vargas [verfasserIn] José Becerra [verfasserIn] José María Reguera [verfasserIn] Ivan Duran [verfasserIn] Fabiana Csukasi [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
acute respiratory distress syndrome |
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| Übergeordnetes Werk: |
In: Frontiers in Immunology - Frontiers Media S.A., 2011, 13(2022) |
|---|---|
| Übergeordnetes Werk: |
volume:13 ; year:2022 |
| Links: |
|---|
| DOI / URN: |
10.3389/fimmu.2022.1054962 |
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| Katalog-ID: |
DOAJ085773956 |
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| 520 | |a Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. | ||
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10.3389/fimmu.2022.1054962 doi (DE-627)DOAJ085773956 (DE-599)DOAJ4dafb99f08e741cf8cd73e3548b14ce6 DE-627 ger DE-627 rakwb eng RC581-607 Gustavo Rico-Llanos verfasserin aut Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. COVID-19 acute respiratory distress syndrome binding-immunoglobulinprotein (BiP/GRP78/HSPA5) cytokine storm cell surface GRP78 (csGRP78) cellular stress Immunologic diseases. Allergy Gustavo Rico-Llanos verfasserin aut Óscar Porras-Perales verfasserin aut Óscar Porras-Perales verfasserin aut Sandra Escalante verfasserin aut Sandra Escalante verfasserin aut Daniel B. Vázquez-Calero verfasserin aut Daniel B. Vázquez-Calero verfasserin aut Lucía Valiente verfasserin aut Lucía Valiente verfasserin aut María I. Castillo verfasserin aut José Miguel Pérez-Tejeiro verfasserin aut José Miguel Pérez-Tejeiro verfasserin aut David Baglietto-Vargas verfasserin aut David Baglietto-Vargas verfasserin aut David Baglietto-Vargas verfasserin aut José Becerra verfasserin aut José Becerra verfasserin aut José Becerra verfasserin aut José María Reguera verfasserin aut José María Reguera verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Fabiana Csukasi verfasserin aut Fabiana Csukasi verfasserin aut Fabiana Csukasi verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 13(2022) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:13 year:2022 https://doi.org/10.3389/fimmu.2022.1054962 kostenfrei https://doaj.org/article/4dafb99f08e741cf8cd73e3548b14ce6 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2022.1054962/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2022 |
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10.3389/fimmu.2022.1054962 doi (DE-627)DOAJ085773956 (DE-599)DOAJ4dafb99f08e741cf8cd73e3548b14ce6 DE-627 ger DE-627 rakwb eng RC581-607 Gustavo Rico-Llanos verfasserin aut Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. COVID-19 acute respiratory distress syndrome binding-immunoglobulinprotein (BiP/GRP78/HSPA5) cytokine storm cell surface GRP78 (csGRP78) cellular stress Immunologic diseases. Allergy Gustavo Rico-Llanos verfasserin aut Óscar Porras-Perales verfasserin aut Óscar Porras-Perales verfasserin aut Sandra Escalante verfasserin aut Sandra Escalante verfasserin aut Daniel B. Vázquez-Calero verfasserin aut Daniel B. Vázquez-Calero verfasserin aut Lucía Valiente verfasserin aut Lucía Valiente verfasserin aut María I. Castillo verfasserin aut José Miguel Pérez-Tejeiro verfasserin aut José Miguel Pérez-Tejeiro verfasserin aut David Baglietto-Vargas verfasserin aut David Baglietto-Vargas verfasserin aut David Baglietto-Vargas verfasserin aut José Becerra verfasserin aut José Becerra verfasserin aut José Becerra verfasserin aut José María Reguera verfasserin aut José María Reguera verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Ivan Duran verfasserin aut Fabiana Csukasi verfasserin aut Fabiana Csukasi verfasserin aut Fabiana Csukasi verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 13(2022) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:13 year:2022 https://doi.org/10.3389/fimmu.2022.1054962 kostenfrei https://doaj.org/article/4dafb99f08e741cf8cd73e3548b14ce6 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2022.1054962/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 13 2022 |
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Gustavo Rico-Llanos @@aut@@ Óscar Porras-Perales @@aut@@ Sandra Escalante @@aut@@ Daniel B. Vázquez-Calero @@aut@@ Lucía Valiente @@aut@@ María I. Castillo @@aut@@ José Miguel Pérez-Tejeiro @@aut@@ David Baglietto-Vargas @@aut@@ José Becerra @@aut@@ José María Reguera @@aut@@ Ivan Duran @@aut@@ Fabiana Csukasi @@aut@@ |
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RC581-607 Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP COVID-19 acute respiratory distress syndrome binding-immunoglobulinprotein (BiP/GRP78/HSPA5) cytokine storm cell surface GRP78 (csGRP78) cellular stress |
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Gustavo Rico-Llanos Óscar Porras-Perales Sandra Escalante Daniel B. Vázquez-Calero Lucía Valiente María I. Castillo José Miguel Pérez-Tejeiro David Baglietto-Vargas José Becerra José María Reguera Ivan Duran Fabiana Csukasi |
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Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP |
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Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. |
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Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. |
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Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show that BiP serum levels are higher in COVID-19 patients who present certain risk factors. Moreover, early during the infection, BiP levels predict severe pneumonia, supporting the use of BiP as a prognosis biomarker. Using a mouse model of pulmonary inflammation, we observed increased levels of cell surface BiP (cs-BiP) in leukocytes during inflammation. This corresponds with a higher number of neutrophiles, which show naturally high levels of cs-BiP, whereas alveolar macrophages show a higher than usual exposure of BiP in their cell surface. The modulation of cellular stress with the use of a clinically approved drug, 4-PBA, resulted in the amelioration of the lung hyperinflammatory response, supporting the anti-stress therapy as a valid therapeutic strategy for patients developing ARDS. Finally, we identified stress-modulated proteins that shed light into the mechanism underlying the cellular stress-inflammation network in lungs. |
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