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Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

ABSTRACT: Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

PROVIDER: PRJNA1199076 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31808389_1.fastq.gz	Fastqsanger.gz
	SRR31808389_2.fastq.gz	Fastqsanger.gz
	SRR31808390_1.fastq.gz	Fastqsanger.gz
	SRR31808390_2.fastq.gz	Fastqsanger.gz
	SRR31808391.fastq.gz	Fastqsanger.gz

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Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [ST]

Project description:Our study confirms that gut microbiota is essential for motor dysfunction and neuropathology in LRRK2 G2019S mice. Monoculturing Parabacteroides goldsteinii mitigates age-related motor dysfunction, alpha-synuclein expression, neuroinflammation, and dopaminergic degeneration. Its effects on the gut microenvironment include suppressing the toll-like receptor 4 signaling pathway, facilitating the differentiation of intestinal dendritic cells and macrophages, and promoting anti-inflammatory intraepithelial CD4+ CD8αα+ T cells. It also upregulates tissue repair and immune differentiation pathways, enhances intestinal epithelial junction and mitochondrial function genes, and reduces colonic alpha-synuclein levels.

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Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

Project description:Evidence suggests that Lewy body pathology in Parkinson's disease (PD) may originate in the gut, with intestinal inflammation serving as an early mediator via the gut-brain axis. Mutations in leucine-rich repeat kinase 2 (LRRK2) are a common genetic risk factor for both PD and inflammatory bowel disease. We proposed that modulating the gut microenvironment could assist in mitigating PD progression, particularly in individuals with LRRK2 mutations. Our study indicates that germ-free condition could only partially alleviate PD process in LRRK2 G2019S mice. Mono-inoculation of PG in germ-free LRRK2 G2019S mice mitigated age-dependent motor dysfunction. In the brain, the colonic P. goldsteinii treatment reduces neuronal a-synuclein expression, ease neuroinflammation, and mitigates dopaminergic degeneration. In the gut, the PG administration suppressed the toll-like receptor 4 signaling, facilitated the differentiation of intestinal dendritic cells and macrophages, and increased the abundance of anti-inflammatory T cells. Our findings demonstrated that colonization by P. goldsteinii alleviates the progression of PD by exerting multifaceted effects in maintaining intestinal homeostasis.

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