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H.pylori infections induces a transcriptional signature in gastric eosinophils, as determined by RNA sequencing

ABSTRACT: H.pylori infections induces a transcriptional signature in gastric eosinophils, as determined by RNA sequencing

PROVIDER: PRJNA414920 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6188790_1.fastq.gz	Fastqsanger.gz
	SRR6188790_2.fastq.gz	Fastqsanger.gz
	SRR6188800_1.fastq.gz	Fastqsanger.gz
	SRR6188800_2.fastq.gz	Fastqsanger.gz
	SRR6188791_1.fastq.gz	Fastqsanger.gz

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H.pylori infections induces a transcriptional signature in gastric eosinophils, as determined by RNA sequencing

Project description:Eosinophils are highly abundant throughout the gastrointestinal tract. However, their function in bacterially-induced gastrointestinal inflammatory disorders is poorly understood. In this study, we have examined the function and regulation of gastric eosinophils in the steady state and during infection with Helicobacter pylori. We find that eosinophils are recruited to sites of infection, make direct contact with live bacteria, and activate a signature transcriptional program.

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Expression profiling of lncRNAs/mRNA for H.pylori infected normal gastric epithelial cell line

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Project description:The recognition of the immune system as a key component of the tumor microenvironment (TME) led to promising therapeutics. Since such therapies benefit only subsets of patients, understanding the activities of immune cells in the TME is required. Eosinophils are an integral part of the TME especially in mucosal tumors. Nonetheless, their role in the TME and the environmental cues that direct their activities are largely unknown, especially in metastasis. We report that breast cancer-driven lung metastasis is characterized by resident and recruited eosinophils. Eosinophil recruitment to the metastatic lung was regulated by G protein coupled receptor signaling but independent of CCR3. Functionally, eosinophils promoted lymphocyte-mediated anti tumor immunity. Transcriptome and proteomic analyses identified the TME rather than intrinsic differences between eosinophil subsets as a key instructing factor directing anti tumorigenic eosinophil activities. Specifically, TNF-a/IFN-g-activated eosinophils facilitated CD4+ and CD8+ T cell infiltration and promoted anti-tumor immunity. Collectively, we identify a mechanism by which the TME entrains eosinophils to adopt anti-tumorigenic properties, which may lead to the development of eosinophil-targeted therapeutics.

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Project description:Purpose: we aimed to characterized the transcriptional profile of mouse eosinophils in response to stimuli that are associated with Type 1 and Type 2 environments Methods: Eosinophils were purified from the peritoneal cavity of Il5Tg mice and stimulated with IL-4 (i.e. type 2 activated eosinophils), IFN-γ, and a combination of lipopolysaccharide (LPS, i.e. type 1 activated eosinophils) in the presence of IFN-γ. Thereafter, RNA was obtained and the transcriptome signature following each stimulation was determined using RNA sequencing. Raw sequencing reads were trimmed and filtered using fastp, then aligned to mouse genome assembly (GRCm38) using STAR 2.7.2a. Normalization and differential expression analysis were performed in R 4.0.3 using the package DESeq2. Finally, gene ontology annotations were obtained from Ensembl and pathway graphs were obtained from KEGG. Results: RNAseq analysis revealed marked differences, which were driven by the different stimulating conditions Conclusion: We demonstrate that eosinophils are polarized to distinct phenotypes following distinct stimuli. These findings contribute to the growing understanding regarding the heterogeneity of eosinophils and their possible roles in different diseases.

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