H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice

Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans<...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Corentin Dumortier [verfasserIn] Rogatien Charlet [verfasserIn] Ali Bettaieb [verfasserIn] Samir Jawhara [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	H89 microbiota

Übergeordnetes Werk:	In: Microorganisms - MDPI AG, 2013, 8(2020), 12, p 2039
Übergeordnetes Werk:	volume:8 ; year:2020 ; number:12, p 2039

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/microorganisms8122039

Katalog-ID:	DOAJ016823079

Internformat


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520			\|a Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut.
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allfields	10.3390/microorganisms8122039 doi (DE-627)DOAJ016823079 (DE-599)DOAJa6b6beb6ccae411290bd17d9e5b2c2c6 DE-627 ger DE-627 rakwb eng QH301-705.5 Corentin Dumortier verfasserin aut H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota Biology (General) Rogatien Charlet verfasserin aut Ali Bettaieb verfasserin aut Samir Jawhara verfasserin aut In Microorganisms MDPI AG, 2013 8(2020), 12, p 2039 (DE-627)750370696 (DE-600)2720891-6 20762607 nnns volume:8 year:2020 number:12, p 2039 https://doi.org/10.3390/microorganisms8122039 kostenfrei https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 kostenfrei https://www.mdpi.com/2076-2607/8/12/2039 kostenfrei https://doaj.org/toc/2076-2607 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2020 12, p 2039
spelling	10.3390/microorganisms8122039 doi (DE-627)DOAJ016823079 (DE-599)DOAJa6b6beb6ccae411290bd17d9e5b2c2c6 DE-627 ger DE-627 rakwb eng QH301-705.5 Corentin Dumortier verfasserin aut H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota Biology (General) Rogatien Charlet verfasserin aut Ali Bettaieb verfasserin aut Samir Jawhara verfasserin aut In Microorganisms MDPI AG, 2013 8(2020), 12, p 2039 (DE-627)750370696 (DE-600)2720891-6 20762607 nnns volume:8 year:2020 number:12, p 2039 https://doi.org/10.3390/microorganisms8122039 kostenfrei https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 kostenfrei https://www.mdpi.com/2076-2607/8/12/2039 kostenfrei https://doaj.org/toc/2076-2607 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2020 12, p 2039
allfields_unstemmed	10.3390/microorganisms8122039 doi (DE-627)DOAJ016823079 (DE-599)DOAJa6b6beb6ccae411290bd17d9e5b2c2c6 DE-627 ger DE-627 rakwb eng QH301-705.5 Corentin Dumortier verfasserin aut H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota Biology (General) Rogatien Charlet verfasserin aut Ali Bettaieb verfasserin aut Samir Jawhara verfasserin aut In Microorganisms MDPI AG, 2013 8(2020), 12, p 2039 (DE-627)750370696 (DE-600)2720891-6 20762607 nnns volume:8 year:2020 number:12, p 2039 https://doi.org/10.3390/microorganisms8122039 kostenfrei https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 kostenfrei https://www.mdpi.com/2076-2607/8/12/2039 kostenfrei https://doaj.org/toc/2076-2607 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2020 12, p 2039
allfieldsGer	10.3390/microorganisms8122039 doi (DE-627)DOAJ016823079 (DE-599)DOAJa6b6beb6ccae411290bd17d9e5b2c2c6 DE-627 ger DE-627 rakwb eng QH301-705.5 Corentin Dumortier verfasserin aut H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota Biology (General) Rogatien Charlet verfasserin aut Ali Bettaieb verfasserin aut Samir Jawhara verfasserin aut In Microorganisms MDPI AG, 2013 8(2020), 12, p 2039 (DE-627)750370696 (DE-600)2720891-6 20762607 nnns volume:8 year:2020 number:12, p 2039 https://doi.org/10.3390/microorganisms8122039 kostenfrei https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 kostenfrei https://www.mdpi.com/2076-2607/8/12/2039 kostenfrei https://doaj.org/toc/2076-2607 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2020 12, p 2039
allfieldsSound	10.3390/microorganisms8122039 doi (DE-627)DOAJ016823079 (DE-599)DOAJa6b6beb6ccae411290bd17d9e5b2c2c6 DE-627 ger DE-627 rakwb eng QH301-705.5 Corentin Dumortier verfasserin aut H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota Biology (General) Rogatien Charlet verfasserin aut Ali Bettaieb verfasserin aut Samir Jawhara verfasserin aut In Microorganisms MDPI AG, 2013 8(2020), 12, p 2039 (DE-627)750370696 (DE-600)2720891-6 20762607 nnns volume:8 year:2020 number:12, p 2039 https://doi.org/10.3390/microorganisms8122039 kostenfrei https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 kostenfrei https://www.mdpi.com/2076-2607/8/12/2039 kostenfrei https://doaj.org/toc/2076-2607 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2020 12, p 2039
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callnumber-first	Q - Science
author	Corentin Dumortier
spellingShingle	Corentin Dumortier misc QH301-705.5 misc H89 misc <i<Candida albicans</i< misc <i<Escherichia coli</i< misc <i<Enterococcus faecalis</i< misc <i<Lactobacillus johnsonii</i< misc microbiota misc Biology (General) H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice
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topic_title	QH301-705.5 H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice H89 <i<Candida albicans</i< <i<Escherichia coli</i< <i<Enterococcus faecalis</i< <i<Lactobacillus johnsonii</i< microbiota
topic	misc QH301-705.5 misc H89 misc <i<Candida albicans</i< misc <i<Escherichia coli</i< misc <i<Enterococcus faecalis</i< misc <i<Lactobacillus johnsonii</i< misc microbiota misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc H89 misc <i<Candida albicans</i< misc <i<Escherichia coli</i< misc <i<Enterococcus faecalis</i< misc <i<Lactobacillus johnsonii</i< misc microbiota misc Biology (General)
topic_browse	misc QH301-705.5 misc H89 misc <i<Candida albicans</i< misc <i<Escherichia coli</i< misc <i<Enterococcus faecalis</i< misc <i<Lactobacillus johnsonii</i< misc microbiota misc Biology (General)
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title	H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice
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title_sort	h89 treatment reduces intestinal inflammation and <i<candida albicans</i< overgrowth in mice
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title_auth	H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice
abstract	Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut.
abstractGer	Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut.
abstract_unstemmed	Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus <i<Candida albicans</i<. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to <i<C. albicans</i< through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and <i<C. albicans</i< clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to <i<C. albicans</i< through DSS-challenged Caco-2 cells. In addition, H89 decreased <i<C. albicans</i< viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of <i<C. albicans</i< from the gut. H89 administration to mice decreased the overgrowth of <i<Escherichia coli</i< and <i<Enterococcus faecalis</i< populations while <i<Lactobacillus johnsonii</i< populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of <i<C. albicans</i< from the gut.
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container_issue	12, p 2039
title_short	H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice
url	https://doi.org/10.3390/microorganisms8122039 https://doaj.org/article/a6b6beb6ccae411290bd17d9e5b2c2c6 https://www.mdpi.com/2076-2607/8/12/2039 https://doaj.org/toc/2076-2607
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H89 Treatment Reduces Intestinal Inflammation and <i<Candida albicans</i< Overgrowth in Mice

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