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ABSTRACT: Cannabinoids modulate the microbiota-gut-brain axis in HIV/SIV infection through reducing neuroinflammation and microbiome alterations while concurrently elevating endocannabinoid and indole-3-propionate levels

PROVIDER: PRJNA926599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23193602_1.fastq.gz	Fastqsanger.gz
	SRR23193602_2.fastq.gz	Fastqsanger.gz
	SRR23193603_1.fastq.gz	Fastqsanger.gz
	SRR23193603_2.fastq.gz	Fastqsanger.gz
	SRR23193604_1.fastq.gz	Fastqsanger.gz

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Project description:The dysregulation of the microbiota-gut-brain axis (MGBA) in people living with HIV (PLWH) consequent to gastrointestinal dysfunction (dysbiosis) can lead to neuroinflammation and persistent cognitive impairment, which underscores the need for new treatments. Here, we show that delta-9-tetrahydrocannabinol (THC) reduced neuroinflammation and microbiome alterations and enhanced plasma endocannabinoid, endocannabinoid-like and indole-3-propionate levels in chronically SIV-infected rhesus macaques. Long-term low-dose THC potently blocked expression of genes associated with type I interferon responses and excitotoxicity (SLC7A11) and enhanced protein expression of WFS1 (endoplasmic reticulum stress) and CRYM (oxidative stress) in basal ganglia. Additionally, THC successfully countered miR-142-3p mediated suppression of WFS1 via a CB1R mediated mechanism in HCN2 neuronal cells. Most importantly, THC increased the relative abundance of Firmicutes and Clostridia including IPA producersing C. botulinum, C. paraputrificum, C. cadaveris and butyrate producersing C. butyricum, Faecalibacterium prauzsnitzii and Butyricicoccus pullicaecorum in the colon. This study highlights low-dose THC as a potential disease-modifying agent that can positively modulate the MGBA by concurrently reducing neuroinflammation and promoting the growth of gut microbial species that produce neuroprotective metabolites like indole-3-propionate in PLWH HIV and other neurodegenerative diseases, thus meriting clinical trials.

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Project description:The study describes miRNA expression in colonic epithelium of chronic SIV-infected rhesus macaques. We profiled and characterized miRNA/mRNA expression exclusively in colonic epithelium (CE) of 12 chronically SIV-infected and 8 control rhesus macaques (RMs). About 46 miRNAs were differentially expressed (DE) (20-up and 26-down) in CE during chronic SIV infection. Using TargetScan, we bioinformatically crossed the predicted targets of DE miRNAs to genome-wide transcriptomic data and identified several critical miRNA-mRNA pairings that suggested miRNA-mediated regulation of aberrant epithelial gene expression in CE. Immunofluorescence, luciferase reporter and miRNA overexpression studies confirmed the ability of miR-130a and miR-212 to bind the 3’ UTR and downregulate protein expression of occludin (OCLN) and peroxisome proliferator activator receptor gamma (PPAR), respectively, two proteins with pivotal roles in epithelial barrier function. MiR-130a and miR-212 overexpression in Caco-2 cells significantly reduced transepithelial electrical resistance (TEER). Interestingly, delta-9-tetrahydrocannabinol (9-THC) treatment restored TEER to levels observed with control miRNA mimic. Finally, ex-vivo 9-THC treatment of colon tissue from chronically SIV-infected RMs significantly increased PPAR gene expression. Our findings suggest that dysregulated miR-130a and miR-212 expression in CE during chronic HIV/SIV infection can facilitate epithelial barrier disruption by downregulating OCLN and PPAR protein expression. Most importantly, our results highlight the beneficial effects of cannabinoids on epithelial barrier function in not just HIV/SIV but potentially other chronic intestinal inflammatory diseases.

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