LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota
Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yan, Jing [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt - Redwan, Mostafa ELSEVIER, 2017transfer abstract, an international journal for analysis of the human and other genomes, San Diego, Calif |
|---|---|
| Übergeordnetes Werk: |
volume:114 ; year:2022 ; number:6 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.ygeno.2022.110527 |
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| 520 | |a Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. | ||
| 520 | |a Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. | ||
| 700 | 1 | |a Yu, Wei |4 oth | |
| 700 | 1 | |a Wang, Guoliang |4 oth | |
| 700 | 1 | |a Lu, Chang |4 oth | |
| 700 | 1 | |a Liu, Chen |4 oth | |
| 700 | 1 | |a Jiang, Lu |4 oth | |
| 700 | 1 | |a Jiang, Zizheng |4 oth | |
| 700 | 1 | |a Liang, Zhenghao |4 oth | |
| 700 | 1 | |a Liu, Dong |4 oth | |
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10.1016/j.ygeno.2022.110527 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001987.pica (DE-627)ELV059804017 (ELSEVIER)S0888-7543(22)00272-5 DE-627 ger DE-627 rakwb eng 550 VZ 620 VZ 55.50 bkl 55.60 bkl 55.60 bkl Yan, Jing verfasserin aut LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Yu, Wei oth Wang, Guoliang oth Lu, Chang oth Liu, Chen oth Jiang, Lu oth Jiang, Zizheng oth Liang, Zhenghao oth Liu, Dong oth Enthalten in Academic Press Redwan, Mostafa ELSEVIER Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt 2017transfer abstract an international journal for analysis of the human and other genomes San Diego, Calif (DE-627)ELV020260245 volume:114 year:2022 number:6 pages:0 https://doi.org/10.1016/j.ygeno.2022.110527 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-AST 55.50 Luftfahrzeugtechnik VZ 55.60 Raumfahrttechnik VZ 55.60 Raumfahrttechnik VZ AR 114 2022 6 0 |
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10.1016/j.ygeno.2022.110527 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001987.pica (DE-627)ELV059804017 (ELSEVIER)S0888-7543(22)00272-5 DE-627 ger DE-627 rakwb eng 550 VZ 620 VZ 55.50 bkl 55.60 bkl 55.60 bkl Yan, Jing verfasserin aut LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Yu, Wei oth Wang, Guoliang oth Lu, Chang oth Liu, Chen oth Jiang, Lu oth Jiang, Zizheng oth Liang, Zhenghao oth Liu, Dong oth Enthalten in Academic Press Redwan, Mostafa ELSEVIER Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt 2017transfer abstract an international journal for analysis of the human and other genomes San Diego, Calif (DE-627)ELV020260245 volume:114 year:2022 number:6 pages:0 https://doi.org/10.1016/j.ygeno.2022.110527 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-AST 55.50 Luftfahrzeugtechnik VZ 55.60 Raumfahrttechnik VZ 55.60 Raumfahrttechnik VZ AR 114 2022 6 0 |
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10.1016/j.ygeno.2022.110527 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001987.pica (DE-627)ELV059804017 (ELSEVIER)S0888-7543(22)00272-5 DE-627 ger DE-627 rakwb eng 550 VZ 620 VZ 55.50 bkl 55.60 bkl 55.60 bkl Yan, Jing verfasserin aut LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Yu, Wei oth Wang, Guoliang oth Lu, Chang oth Liu, Chen oth Jiang, Lu oth Jiang, Zizheng oth Liang, Zhenghao oth Liu, Dong oth Enthalten in Academic Press Redwan, Mostafa ELSEVIER Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt 2017transfer abstract an international journal for analysis of the human and other genomes San Diego, Calif (DE-627)ELV020260245 volume:114 year:2022 number:6 pages:0 https://doi.org/10.1016/j.ygeno.2022.110527 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-AST 55.50 Luftfahrzeugtechnik VZ 55.60 Raumfahrttechnik VZ 55.60 Raumfahrttechnik VZ AR 114 2022 6 0 |
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10.1016/j.ygeno.2022.110527 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001987.pica (DE-627)ELV059804017 (ELSEVIER)S0888-7543(22)00272-5 DE-627 ger DE-627 rakwb eng 550 VZ 620 VZ 55.50 bkl 55.60 bkl 55.60 bkl Yan, Jing verfasserin aut LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Yu, Wei oth Wang, Guoliang oth Lu, Chang oth Liu, Chen oth Jiang, Lu oth Jiang, Zizheng oth Liang, Zhenghao oth Liu, Dong oth Enthalten in Academic Press Redwan, Mostafa ELSEVIER Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt 2017transfer abstract an international journal for analysis of the human and other genomes San Diego, Calif (DE-627)ELV020260245 volume:114 year:2022 number:6 pages:0 https://doi.org/10.1016/j.ygeno.2022.110527 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-AST 55.50 Luftfahrzeugtechnik VZ 55.60 Raumfahrttechnik VZ 55.60 Raumfahrttechnik VZ AR 114 2022 6 0 |
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10.1016/j.ygeno.2022.110527 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001987.pica (DE-627)ELV059804017 (ELSEVIER)S0888-7543(22)00272-5 DE-627 ger DE-627 rakwb eng 550 VZ 620 VZ 55.50 bkl 55.60 bkl 55.60 bkl Yan, Jing verfasserin aut LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. Yu, Wei oth Wang, Guoliang oth Lu, Chang oth Liu, Chen oth Jiang, Lu oth Jiang, Zizheng oth Liang, Zhenghao oth Liu, Dong oth Enthalten in Academic Press Redwan, Mostafa ELSEVIER Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt 2017transfer abstract an international journal for analysis of the human and other genomes San Diego, Calif (DE-627)ELV020260245 volume:114 year:2022 number:6 pages:0 https://doi.org/10.1016/j.ygeno.2022.110527 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-AST 55.50 Luftfahrzeugtechnik VZ 55.60 Raumfahrttechnik VZ 55.60 Raumfahrttechnik VZ AR 114 2022 6 0 |
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Enthalten in Flood hazard assessment and heavy metal distributions around Um Gheig mine area, Eastern Desert, Egypt San Diego, Calif volume:114 year:2022 number:6 pages:0 |
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lrrk2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota |
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LRRK2 deficiency mitigates colitis progression by favoring resolution of inflammation and restoring homeostasis of gut microbiota |
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Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. |
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Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. |
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Leucine rich-repeat kinase 2 (LRRK2) has been considered a susceptibility gene for ulcerative colitis (UC), and its protein abundance was enhanced in the peripheral blood mononuclear cells (PBMCs) from UC cohorts as compared to healthy volunteers. In preclinical models of colitis, Lrrk2 deficiency ameliorated dextran sodium sulfate (DSS)-induced colitis progression, whereas the processes were aggravated by R1441C mutation. While intestinal macrophages (MФs) from Lrrk2 knock-out (Lrrk2 −/− ) mice exhibited a tendency to transit to alternatively activated MФs, R1441C MФs mutation facilitated the pro-inflammatory phenotype polarization, determined by RNA sequencing and qPCR. Moreover, we characterized their microbiota profiles and found that loss of Lrrk2 increased the bacterial richness and altered bacterial community structure, and this shift contributed to the alleviation of colitis development and progression. We proposed that Lrrk2 deficiency promotes M2 MФ transition and facilitates probiotics colonization, providing a protective role during colitis. |
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