Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1281861 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR34170402_1.fastq.gz | Fastqsanger.gz | |||
| SRR34170402_2.fastq.gz | Fastqsanger.gz | |||
| SRR34170403_1.fastq.gz | Fastqsanger.gz | |||
| SRR34170403_2.fastq.gz | Fastqsanger.gz |
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Project description:Global transcriptional responses in duodenal intestinal epithelia of chickens following primary and secondary Eimeria acervulina infections. Simple loop hybridization (day 0 vs. days 1-2, days 1-2 vs. 3-4, days 3-4 vs. 5-6, and days 5-6 vs. 7-8) per primary or secondary infections.
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Project description:Global transcriptional responses in duodenal intestinal epithelia of chickens following primary and secondary Eimeria acervulina infections.
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Project description:The gut microbiome plays a crucial role in modulating human immunity. Previously, we found that antibiotic-induced microbiome perturbation affected influenza vaccine responses depending on pre-existing immunity levels. However, its impact on primary responses remains unclear. Here, we employed a systems biology approach to analyze the impact of antibiotic administration on primary and secondary immune responses to the rabies vaccine in humans. Antibiotic administration disrupted the microbiome, reducing gut bacterial load and causing long-lasting reduction in commensal diversity. This alteration was associated with reduced rabies-specific humoral responses. Multi-omics profiling revealed that antibiotic administration induced: 1) an enhanced pro-inflammatory signature early after vaccination, 2) a shift in the balance of vaccine-specific T-helper 1(Th1) to T-follicular-helper response towards Th1 phenotype, 3) profound alterations in metabolites, particularly in secondary bile acids in blood. By integrating multi-omics datasets, we generated a multi-scale, multi-response network that revealed key regulatory nodes including the microbiota, secondary bile acids, and humoral immunity to vaccination.
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Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
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