Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease.
The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from un...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Melanie Ricke-Hoch [verfasserIn] Elisabeth Stelling [verfasserIn] Lisa Lasswitz [verfasserIn] Antonia P Gunesch [verfasserIn] Martina Kasten [verfasserIn] Francisco J Zapatero-Belinchón [verfasserIn] Graham Brogden [verfasserIn] Gisa Gerold [verfasserIn] Thomas Pietschmann [verfasserIn] Virginie Montiel [verfasserIn] Jean-Luc Balligand [verfasserIn] Federica Facciotti [verfasserIn] Emilio Hirsch [verfasserIn] Thomas Gausepohl [verfasserIn] Husni Elbahesh [verfasserIn] Guus F Rimmelzwaan [verfasserIn] Anne Höfer [verfasserIn] Mark P Kühnel [verfasserIn] Danny Jonigk [verfasserIn] Julian Eigendorf [verfasserIn] Uwe Tegtbur [verfasserIn] Lena Mink [verfasserIn] Michaela Scherr [verfasserIn] Thomas Illig [verfasserIn] Axel Schambach [verfasserIn] Tobias J Pfeffer [verfasserIn] Andres Hilfiker [verfasserIn] Axel Haverich [verfasserIn] Denise Hilfiker-Kleiner [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Übergeordnetes Werk: |
In: PLoS ONE - Public Library of Science (PLoS), 2007, 16(2021), 8, p e0255335 |
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| Übergeordnetes Werk: |
volume:16 ; year:2021 ; number:8, p e0255335 |
| Links: |
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| DOI / URN: |
10.1371/journal.pone.0255335 |
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DOAJ072314125 |
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| 520 | |a The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. | ||
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10.1371/journal.pone.0255335 doi (DE-627)DOAJ072314125 (DE-599)DOAJ29020b7734ec4bb5ae0e7a607b498ae0 DE-627 ger DE-627 rakwb eng Melanie Ricke-Hoch verfasserin aut Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. Medicine R Science Q Elisabeth Stelling verfasserin aut Lisa Lasswitz verfasserin aut Antonia P Gunesch verfasserin aut Martina Kasten verfasserin aut Francisco J Zapatero-Belinchón verfasserin aut Graham Brogden verfasserin aut Gisa Gerold verfasserin aut Thomas Pietschmann verfasserin aut Virginie Montiel verfasserin aut Jean-Luc Balligand verfasserin aut Federica Facciotti verfasserin aut Emilio Hirsch verfasserin aut Thomas Gausepohl verfasserin aut Husni Elbahesh verfasserin aut Guus F Rimmelzwaan verfasserin aut Anne Höfer verfasserin aut Mark P Kühnel verfasserin aut Danny Jonigk verfasserin aut Julian Eigendorf verfasserin aut Uwe Tegtbur verfasserin aut Lena Mink verfasserin aut Michaela Scherr verfasserin aut Thomas Illig verfasserin aut Axel Schambach verfasserin aut Tobias J Pfeffer verfasserin aut Andres Hilfiker verfasserin aut Axel Haverich verfasserin aut Denise Hilfiker-Kleiner verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 16(2021), 8, p e0255335 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:16 year:2021 number:8, p e0255335 https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/article/29020b7734ec4bb5ae0e7a607b498ae0 kostenfrei https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/toc/1932-6203 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_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 8, p e0255335 |
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10.1371/journal.pone.0255335 doi (DE-627)DOAJ072314125 (DE-599)DOAJ29020b7734ec4bb5ae0e7a607b498ae0 DE-627 ger DE-627 rakwb eng Melanie Ricke-Hoch verfasserin aut Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. Medicine R Science Q Elisabeth Stelling verfasserin aut Lisa Lasswitz verfasserin aut Antonia P Gunesch verfasserin aut Martina Kasten verfasserin aut Francisco J Zapatero-Belinchón verfasserin aut Graham Brogden verfasserin aut Gisa Gerold verfasserin aut Thomas Pietschmann verfasserin aut Virginie Montiel verfasserin aut Jean-Luc Balligand verfasserin aut Federica Facciotti verfasserin aut Emilio Hirsch verfasserin aut Thomas Gausepohl verfasserin aut Husni Elbahesh verfasserin aut Guus F Rimmelzwaan verfasserin aut Anne Höfer verfasserin aut Mark P Kühnel verfasserin aut Danny Jonigk verfasserin aut Julian Eigendorf verfasserin aut Uwe Tegtbur verfasserin aut Lena Mink verfasserin aut Michaela Scherr verfasserin aut Thomas Illig verfasserin aut Axel Schambach verfasserin aut Tobias J Pfeffer verfasserin aut Andres Hilfiker verfasserin aut Axel Haverich verfasserin aut Denise Hilfiker-Kleiner verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 16(2021), 8, p e0255335 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:16 year:2021 number:8, p e0255335 https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/article/29020b7734ec4bb5ae0e7a607b498ae0 kostenfrei https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/toc/1932-6203 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_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 8, p e0255335 |
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10.1371/journal.pone.0255335 doi (DE-627)DOAJ072314125 (DE-599)DOAJ29020b7734ec4bb5ae0e7a607b498ae0 DE-627 ger DE-627 rakwb eng Melanie Ricke-Hoch verfasserin aut Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. Medicine R Science Q Elisabeth Stelling verfasserin aut Lisa Lasswitz verfasserin aut Antonia P Gunesch verfasserin aut Martina Kasten verfasserin aut Francisco J Zapatero-Belinchón verfasserin aut Graham Brogden verfasserin aut Gisa Gerold verfasserin aut Thomas Pietschmann verfasserin aut Virginie Montiel verfasserin aut Jean-Luc Balligand verfasserin aut Federica Facciotti verfasserin aut Emilio Hirsch verfasserin aut Thomas Gausepohl verfasserin aut Husni Elbahesh verfasserin aut Guus F Rimmelzwaan verfasserin aut Anne Höfer verfasserin aut Mark P Kühnel verfasserin aut Danny Jonigk verfasserin aut Julian Eigendorf verfasserin aut Uwe Tegtbur verfasserin aut Lena Mink verfasserin aut Michaela Scherr verfasserin aut Thomas Illig verfasserin aut Axel Schambach verfasserin aut Tobias J Pfeffer verfasserin aut Andres Hilfiker verfasserin aut Axel Haverich verfasserin aut Denise Hilfiker-Kleiner verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 16(2021), 8, p e0255335 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:16 year:2021 number:8, p e0255335 https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/article/29020b7734ec4bb5ae0e7a607b498ae0 kostenfrei https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/toc/1932-6203 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_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 8, p e0255335 |
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10.1371/journal.pone.0255335 doi (DE-627)DOAJ072314125 (DE-599)DOAJ29020b7734ec4bb5ae0e7a607b498ae0 DE-627 ger DE-627 rakwb eng Melanie Ricke-Hoch verfasserin aut Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. Medicine R Science Q Elisabeth Stelling verfasserin aut Lisa Lasswitz verfasserin aut Antonia P Gunesch verfasserin aut Martina Kasten verfasserin aut Francisco J Zapatero-Belinchón verfasserin aut Graham Brogden verfasserin aut Gisa Gerold verfasserin aut Thomas Pietschmann verfasserin aut Virginie Montiel verfasserin aut Jean-Luc Balligand verfasserin aut Federica Facciotti verfasserin aut Emilio Hirsch verfasserin aut Thomas Gausepohl verfasserin aut Husni Elbahesh verfasserin aut Guus F Rimmelzwaan verfasserin aut Anne Höfer verfasserin aut Mark P Kühnel verfasserin aut Danny Jonigk verfasserin aut Julian Eigendorf verfasserin aut Uwe Tegtbur verfasserin aut Lena Mink verfasserin aut Michaela Scherr verfasserin aut Thomas Illig verfasserin aut Axel Schambach verfasserin aut Tobias J Pfeffer verfasserin aut Andres Hilfiker verfasserin aut Axel Haverich verfasserin aut Denise Hilfiker-Kleiner verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 16(2021), 8, p e0255335 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:16 year:2021 number:8, p e0255335 https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/article/29020b7734ec4bb5ae0e7a607b498ae0 kostenfrei https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/toc/1932-6203 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_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 8, p e0255335 |
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10.1371/journal.pone.0255335 doi (DE-627)DOAJ072314125 (DE-599)DOAJ29020b7734ec4bb5ae0e7a607b498ae0 DE-627 ger DE-627 rakwb eng Melanie Ricke-Hoch verfasserin aut Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. Medicine R Science Q Elisabeth Stelling verfasserin aut Lisa Lasswitz verfasserin aut Antonia P Gunesch verfasserin aut Martina Kasten verfasserin aut Francisco J Zapatero-Belinchón verfasserin aut Graham Brogden verfasserin aut Gisa Gerold verfasserin aut Thomas Pietschmann verfasserin aut Virginie Montiel verfasserin aut Jean-Luc Balligand verfasserin aut Federica Facciotti verfasserin aut Emilio Hirsch verfasserin aut Thomas Gausepohl verfasserin aut Husni Elbahesh verfasserin aut Guus F Rimmelzwaan verfasserin aut Anne Höfer verfasserin aut Mark P Kühnel verfasserin aut Danny Jonigk verfasserin aut Julian Eigendorf verfasserin aut Uwe Tegtbur verfasserin aut Lena Mink verfasserin aut Michaela Scherr verfasserin aut Thomas Illig verfasserin aut Axel Schambach verfasserin aut Tobias J Pfeffer verfasserin aut Andres Hilfiker verfasserin aut Axel Haverich verfasserin aut Denise Hilfiker-Kleiner verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 16(2021), 8, p e0255335 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:16 year:2021 number:8, p e0255335 https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/article/29020b7734ec4bb5ae0e7a607b498ae0 kostenfrei https://doi.org/10.1371/journal.pone.0255335 kostenfrei https://doaj.org/toc/1932-6203 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_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 8, p e0255335 |
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Melanie Ricke-Hoch @@aut@@ Elisabeth Stelling @@aut@@ Lisa Lasswitz @@aut@@ Antonia P Gunesch @@aut@@ Martina Kasten @@aut@@ Francisco J Zapatero-Belinchón @@aut@@ Graham Brogden @@aut@@ Gisa Gerold @@aut@@ Thomas Pietschmann @@aut@@ Virginie Montiel @@aut@@ Jean-Luc Balligand @@aut@@ Federica Facciotti @@aut@@ Emilio Hirsch @@aut@@ Thomas Gausepohl @@aut@@ Husni Elbahesh @@aut@@ Guus F Rimmelzwaan @@aut@@ Anne Höfer @@aut@@ Mark P Kühnel @@aut@@ Danny Jonigk @@aut@@ Julian Eigendorf @@aut@@ Uwe Tegtbur @@aut@@ Lena Mink @@aut@@ Michaela Scherr @@aut@@ Thomas Illig @@aut@@ Axel Schambach @@aut@@ Tobias J Pfeffer @@aut@@ Andres Hilfiker @@aut@@ Axel Haverich @@aut@@ Denise Hilfiker-Kleiner @@aut@@ |
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Melanie Ricke-Hoch |
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Melanie Ricke-Hoch misc Medicine misc R misc Science misc Q Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. |
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Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease |
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impaired immune response mediated by prostaglandin e2 promotes severe covid-19 disease |
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Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. |
| abstract |
The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. |
| abstractGer |
The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. |
| abstract_unstemmed |
The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds that risk-factors for severe COVID-19 disease courses, i.e. male sex, older age and sedentary life style are associated with higher prostaglandin E2 (PGE2) serum levels in blood samples from unaffected subjects. In COVID-19 patients, PGE2 blood levels are markedly elevated and correlate positively with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human precision cut lung slices (PCLS) infected with SARS-CoV-2 display upregulated COX-2. Regular exercise in aged individuals lowers PGE2 serum levels, which leads to increased Paired-Box-Protein-Pax-5 (PAX5) expression, a master regulator of B-cell survival, proliferation and differentiation also towards long lived memory B-cells, in human pre-B-cell lines. Moreover, PGE2 levels in serum of COVID-19 patients lowers the expression of PAX5 in human pre-B-cell lines. The PGE2 inhibitor Taxifolin reduces SARS-CoV-2-induced PGE2 production. In conclusion, SARS-CoV-2, male sex, old age, and sedentary life style increase PGE2 levels, which may reduce the early anti-viral defense as well as the development of immunity promoting severe disease courses and multiple infections. Regular exercise and Taxifolin treatment may reduce these risks and prevent severe disease courses. |
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Impaired immune response mediated by prostaglandin E2 promotes severe COVID-19 disease. |
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