Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis

Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold i...
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Autor*in:	Caitlin V. Lewis [verfasserIn] Hassan Sellak [verfasserIn] Mariem A. Sawan [verfasserIn] Giji Joseph [verfasserIn] Trevor M. Darby [verfasserIn] David VanInsberghe [verfasserIn] Crystal R. Naudin [verfasserIn] David R. Archer [verfasserIn] Rheinallt M. Jones [verfasserIn] W. Robert Taylor [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease

Übergeordnetes Werk:	In: FASEB BioAdvances - Wiley, 2019, 5(2023), 5, Seite 199-210
Übergeordnetes Werk:	volume:5 ; year:2023 ; number:5 ; pages:199-210

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1096/fba.2022-00121

Katalog-ID:	DOAJ090132912

Internformat


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520			\|a Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.
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allfields	10.1096/fba.2022-00121 doi (DE-627)DOAJ090132912 (DE-599)DOAJ286f62f9ca5f48d3a0d039d671dbac67 DE-627 ger DE-627 rakwb eng QH301-705.5 Caitlin V. Lewis verfasserin aut Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine. gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General) Hassan Sellak verfasserin aut Mariem A. Sawan verfasserin aut Giji Joseph verfasserin aut Trevor M. Darby verfasserin aut David VanInsberghe verfasserin aut Crystal R. Naudin verfasserin aut David R. Archer verfasserin aut Rheinallt M. Jones verfasserin aut W. Robert Taylor verfasserin aut In FASEB BioAdvances Wiley, 2019 5(2023), 5, Seite 199-210 (DE-627)1663403198 (DE-600)2969880-7 25739832 nnns volume:5 year:2023 number:5 pages:199-210 https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 kostenfrei https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/toc/2573-9832 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2023 5 199-210
spelling	10.1096/fba.2022-00121 doi (DE-627)DOAJ090132912 (DE-599)DOAJ286f62f9ca5f48d3a0d039d671dbac67 DE-627 ger DE-627 rakwb eng QH301-705.5 Caitlin V. Lewis verfasserin aut Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine. gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General) Hassan Sellak verfasserin aut Mariem A. Sawan verfasserin aut Giji Joseph verfasserin aut Trevor M. Darby verfasserin aut David VanInsberghe verfasserin aut Crystal R. Naudin verfasserin aut David R. Archer verfasserin aut Rheinallt M. Jones verfasserin aut W. Robert Taylor verfasserin aut In FASEB BioAdvances Wiley, 2019 5(2023), 5, Seite 199-210 (DE-627)1663403198 (DE-600)2969880-7 25739832 nnns volume:5 year:2023 number:5 pages:199-210 https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 kostenfrei https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/toc/2573-9832 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2023 5 199-210
allfields_unstemmed	10.1096/fba.2022-00121 doi (DE-627)DOAJ090132912 (DE-599)DOAJ286f62f9ca5f48d3a0d039d671dbac67 DE-627 ger DE-627 rakwb eng QH301-705.5 Caitlin V. Lewis verfasserin aut Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine. gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General) Hassan Sellak verfasserin aut Mariem A. Sawan verfasserin aut Giji Joseph verfasserin aut Trevor M. Darby verfasserin aut David VanInsberghe verfasserin aut Crystal R. Naudin verfasserin aut David R. Archer verfasserin aut Rheinallt M. Jones verfasserin aut W. Robert Taylor verfasserin aut In FASEB BioAdvances Wiley, 2019 5(2023), 5, Seite 199-210 (DE-627)1663403198 (DE-600)2969880-7 25739832 nnns volume:5 year:2023 number:5 pages:199-210 https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 kostenfrei https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/toc/2573-9832 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2023 5 199-210
allfieldsGer	10.1096/fba.2022-00121 doi (DE-627)DOAJ090132912 (DE-599)DOAJ286f62f9ca5f48d3a0d039d671dbac67 DE-627 ger DE-627 rakwb eng QH301-705.5 Caitlin V. Lewis verfasserin aut Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine. gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General) Hassan Sellak verfasserin aut Mariem A. Sawan verfasserin aut Giji Joseph verfasserin aut Trevor M. Darby verfasserin aut David VanInsberghe verfasserin aut Crystal R. Naudin verfasserin aut David R. Archer verfasserin aut Rheinallt M. Jones verfasserin aut W. Robert Taylor verfasserin aut In FASEB BioAdvances Wiley, 2019 5(2023), 5, Seite 199-210 (DE-627)1663403198 (DE-600)2969880-7 25739832 nnns volume:5 year:2023 number:5 pages:199-210 https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 kostenfrei https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/toc/2573-9832 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2023 5 199-210
allfieldsSound	10.1096/fba.2022-00121 doi (DE-627)DOAJ090132912 (DE-599)DOAJ286f62f9ca5f48d3a0d039d671dbac67 DE-627 ger DE-627 rakwb eng QH301-705.5 Caitlin V. Lewis verfasserin aut Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine. gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General) Hassan Sellak verfasserin aut Mariem A. Sawan verfasserin aut Giji Joseph verfasserin aut Trevor M. Darby verfasserin aut David VanInsberghe verfasserin aut Crystal R. Naudin verfasserin aut David R. Archer verfasserin aut Rheinallt M. Jones verfasserin aut W. Robert Taylor verfasserin aut In FASEB BioAdvances Wiley, 2019 5(2023), 5, Seite 199-210 (DE-627)1663403198 (DE-600)2969880-7 25739832 nnns volume:5 year:2023 number:5 pages:199-210 https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 kostenfrei https://doi.org/10.1096/fba.2022-00121 kostenfrei https://doaj.org/toc/2573-9832 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2023 5 199-210
language	English
source	In FASEB BioAdvances 5(2023), 5, Seite 199-210 volume:5 year:2023 number:5 pages:199-210
sourceStr	In FASEB BioAdvances 5(2023), 5, Seite 199-210 volume:5 year:2023 number:5 pages:199-210
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease Biology (General)
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container_title	FASEB BioAdvances
authorswithroles_txt_mv	Caitlin V. Lewis @@aut@@ Hassan Sellak @@aut@@ Mariem A. Sawan @@aut@@ Giji Joseph @@aut@@ Trevor M. Darby @@aut@@ David VanInsberghe @@aut@@ Crystal R. Naudin @@aut@@ David R. Archer @@aut@@ Rheinallt M. Jones @@aut@@ W. Robert Taylor @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
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id	DOAJ090132912
language_de	englisch
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Lewis</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). 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callnumber-first	Q - Science
author	Caitlin V. Lewis
spellingShingle	Caitlin V. Lewis misc QH301-705.5 misc gut microbiome misc intestinal permeability misc neutrophils misc oxidative stress misc sickle cell disease misc Biology (General) Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
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topic_title	QH301-705.5 Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis gut microbiome intestinal permeability neutrophils oxidative stress sickle cell disease
topic	misc QH301-705.5 misc gut microbiome misc intestinal permeability misc neutrophils misc oxidative stress misc sickle cell disease misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc gut microbiome misc intestinal permeability misc neutrophils misc oxidative stress misc sickle cell disease misc Biology (General)
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title	Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
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title_full	Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
author_sort	Caitlin V. Lewis
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author_browse	Caitlin V. Lewis Hassan Sellak Mariem A. Sawan Giji Joseph Trevor M. Darby David VanInsberghe Crystal R. Naudin David R. Archer Rheinallt M. Jones W. Robert Taylor
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title_sort	intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
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title_auth	Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
abstract	Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.
abstractGer	Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.
abstract_unstemmed	Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.
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title_short	Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis
url	https://doi.org/10.1096/fba.2022-00121 https://doaj.org/article/286f62f9ca5f48d3a0d039d671dbac67 https://doaj.org/toc/2573-9832
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up_date	2024-07-04T02:01:31.263Z
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Lewis</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The intestinal microbiome has emerged as a potential contributor to the severity of sickle cell disease (SCD). We sought to determine whether SCD mice exhibit intestinal barrier dysfunction, inflammation, and dysbiosis. Using the Townes humanized sickle cell mouse model, we found a 3‐fold increase in intestinal permeability as assessed via FITC‐dextran (4 kDa) assay in SS (SCD) mice compared to AA (wild type) mice (n = 4, p < 0.05). This was associated with 25 to 50% decreases in claudin‐1, 3, and 15 and zonula occludens‐1 gene expression (n = 8–10, p < 0.05) in the small intestine. Increased Ly6G staining demonstrated more neutrophils in the SS small intestine (3‐fold, n = 5, p < 0.05) associated with increased expression of TNFα, IL‐17A, CXCL1, and CD68 (2.5 to 5‐fold, n = 7–10, p < 0.05). In addition, we observed 30 to 55% decreases in superoxide dismutase‐1, glutathione peroxidase‐1, and catalase antioxidant enzyme expression (n = 7–8, p < 0.05) concomitant to an increase in superoxide (2‐fold, n = 4, p < 0.05). Importantly, all significant observations of a leaky gut phenotype and inflammation were limited to the small intestine and not observed in the colon. Finally, characterization of the composition of the microbiome within the small intestine revealed dysbiosis in SS mice compared to their AA littermates with 47 phyla to species‐level significant alterations in amplicon sequence variants. We conclude that the intestinal barrier is compromised in SCD, associated with decreased gene expression of tight junction proteins, enhanced inflammation, oxidative stress, and gut microbiome dysbiosis, all specific to the small intestine.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">gut microbiome</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">intestinal permeability</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">neutrophils</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">oxidative stress</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">sickle cell disease</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biology (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Hassan Sellak</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Mariem A. 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Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis

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