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Group A Streptococcus M1T1 Intracellular Infection of Primary Tonsil Epithelial Cells Dampens Levels of Secreted IL-8 Through the Action of SpyCEP

ABSTRACT: Group A Streptococcus M1T1 Intracellular Infection of Primary Tonsil Epithelial Cells Dampens Levels of Secreted IL-8 Through the Action of SpyCEP

PROVIDER: PRJNA418763 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6298050.fastq.gz	Fastqsanger.gz
	SRR6298060.fastq.gz	Fastqsanger.gz
	SRR6298070.fastq.gz	Fastqsanger.gz
	SRR6298080.fastq.gz	Fastqsanger.gz
	SRR6298090.fastq.gz	Fastqsanger.gz

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Group A Streptococcus M1T1 Intracellular Infection of Primary Tonsil Epithelial Cells Dampens Levels of Secreted IL-8 Through the Action of SpyCEP

Project description:Streptococcus pyogenes (Group A Streptococcus; GAS) commonly causes pharyngitis in children and adults, with severe invasive disease and immune sequelae being an infrequent consequence. The ability of GAS to invade the host and establish infection likely involves subversion of host immune defenses. However, the signaling pathways and innate immune responses of epithelial cells to GAS are not well understood. In this study, we utilized RNAseq to characterize the inflammatory responses of primary human tonsil epithelial (TEpi) cells to infection with the laboratory-adapted M6 strain JRS4 and the M1T1 clinical isolate 5448. Both strains induced the expression of genes encoding a wide range of inflammatory mediators, including IL-8. Pathway analysis revealed differentially expressed genes between mock and JRS4 or 5448-infected TEpi cells, were enriched in transcription factor networks that regulate IL-8 expression, such as AP-1, ATF-2 and NFAT. While JRS4 infection resulted in high levels of secreted IL-8, 5448 infection did not, suggesting that 5448 may post-transcriptionally dampen IL-8 production. Infection with 5448ΔcepA, an isogenic mutant lacking the IL-8 protease SpyCEP, resulted in IL-8 secretion levels comparable to JRS4 infection. Complementation of 5448ΔcepA and JRS4 with a plasmid encoding 5448-derived SpyCEP significantly reduced IL-8 secretion by TEpi cells. Our results suggest that intracellular infection with the pathogenic GAS M1T1 clone induces a strong pro-inflammatory response in primary tonsil epithelial cells, but modulates this host response by selectively degrading the neutrophil-recruiting chemokine IL-8 to benefit infection.

2018-05-08 | GSE107001 | GEO

Group A Streptococcus M1T1 Intracellular Infection of Primary Tonsil Epithelial Cells Dampens Levels of Secreted IL-8 Through the Action of SpyCEP.

Project description:Streptococcus pyogenes (Group A Streptococcus; GAS) commonly causes pharyngitis in children and adults, with severe invasive disease and immune sequelae being an infrequent consequence. The ability of GAS to invade the host and establish infection likely involves subversion of host immune defenses. However, the signaling pathways and innate immune responses of epithelial cells to GAS are not well-understood. In this study, we utilized RNAseq to characterize the inflammatory responses of primary human tonsil epithelial (TEpi) cells to infection with the laboratory-adapted M6 strain JRS4 and the M1T1 clinical isolate 5448. Both strains induced the expression of genes encoding a wide range of inflammatory mediators, including IL-8. Pathway analysis revealed differentially expressed genes between mock and JRS4- or 5448-infected TEpi cells were enriched in transcription factor networks that regulate IL-8 expression, such as AP-1, ATF-2, and NFAT. While JRS4 infection resulted in high levels of secreted IL-8, 5448 infection did not, suggesting that 5448 may post-transcriptionally dampen IL-8 production. Infection with 5448?cepA, an isogenic mutant lacking the IL-8 protease SpyCEP, resulted in IL-8 secretion levels comparable to JRS4 infection. Complementation of 5448?cepA and JRS4 with a plasmid encoding 5448-derived SpyCEP significantly reduced IL-8 secretion by TEpi cells. Our results suggest that intracellular infection with the pathogenic GAS M1T1 clone induces a strong pro-inflammatory response in primary tonsil epithelial cells, but modulates this host response by selectively degrading the neutrophil-recruiting chemokine IL-8 to benefit infection.

| S-EPMC5966554 | biostudies-literature

Tonsil cancer compared with normal tonsil tissue

Project description:Tonsil cancer compared with normal tonsil tissue

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Tonsil cancer compared with normal tonsil tissue

Project description:To investigate miRNA expression in human tonsil squamous cell carcinoma (SCC) compared to normal tonsil tissue. Two colour LNA Exiqon array. MicroRNAs were labeled at 3'-end with a P-CU-C3-Cy3 RNA linker. A mixture of 371 synthetic DNA reference oligonucleotides containing complementary sequences to all LNA probes was randomly labeled using the ULYSIS labeling kit.

2015-12-23 | GSE75630 | GEO

Lymphe node vs. Tonsil

Project description:Lymph node vs. tonsil Keywords: repeat sample

2005-12-31 | GSE2665 | GEO

Effect of PDGF-Ddstimulation on human tonsil ILC1

Project description:The effect of PDGF-DD on the gene expression of human tonsil ILC1 is unknown. We used microarray to determine the transcriptional differences between unstimulated and PDGF-DD-stimulated human tonsil ILC1.

2018-02-01 | GSE107043 | GEO

Gene expression in tonsil and oral epithelia

Project description:To study characteristics of the orapharyngeal epithelia which may influence susceptibility or resistance to HIV, we performed microarray analysis of the tonsil and gingival epithelium.Tonsil epithelium has been implicated in HIV pathogenesis, but its role in oral transmission remains controversial. We performed microarray analysis of Laser Capture Microdissected tonsil and gingival epithelium. Our data revealed that genes related to immune functions such as antibody production and antigen processing were increasingly expressed in tonsil compared to the epithelium of another oro-pharyngeal site, gingival epithelium. Importantly, tonsil epithelium highly expressed genes associated with HIV entrapment and/or transmission, including the HIV co-receptor CXCR4 and the potential HIV binding molecules, FcRγIII, complement receptor 2, and various complement components. This increased expression of molecules involved in viral recognition, binding and entry may favor virus-epithelium interaction in an environment with reduced innate anti-viral mechanisms. Specifically, secretory leukocyte protease inhibitor, an innate molecule with anti-HIV activity, was minimal in the tonsil epithelium, in contrast to oral mucosa. Collectively, our data suggest that increased expression of molecules associated with HIV binding and entry coupled with decreased innate anti-viral factors may render the tonsil a potential site for oral transmission. Keywords: Cross sectional

2007-12-31 | GSE7224 | GEO

Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs)

Project description:Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs) from three independent tonsil donors.

2016-01-27 | GSE70580 | GEO

Pathochip data of tonsil and lymph node samples

Project description:The Microbiome of HPV-Positive Tonsil Squamous Cell Carcinoma and Neck Metastasis

2021-03-06 | GSE168358 | GEO

Distinct localization, transcriptional profiles, and functionality in early life tonsil regulatory T cells

Project description:CD4+ regulatory T cells (Tregs) are key orchestrators of the immune system, fostering the establishment of protective immunity while preventing deleterious responses. Infancy and childhood are crucial periods of rapid immunologic development but how Tregs mediate immune responses at these earliest timepoints of human life is poorly understood. Here we compare blood and tissue (tonsil) Tregs across pediatric and adult subjects to investigate age related differences in Treg biology. We observed increased FoxP3 expression and proportions of Tregs in tonsil compared to paired blood samples in children. Within tonsil, early life Tregs accumulated in extrafollicular regions with cellular interactions biased towards CD8+ T cells. Tonsil Tregs in both children and adults expressed transcriptional profiles enriched for lineage defining signatures and canonical functionality compared to blood, suggesting tissue as the primary site of Treg activity. Early life tonsil Tregs transcriptional profiles were further defined by pathways associated with activation, proliferation, and polyfunctionality. Observed differences in pediatric tonsil Treg transcriptional signatures were associated with phenotypic differences, high proliferative capacity and robust production of IL-10 compared to adult Tregs. These results identify tissue as a major driver of Treg identity, provide new insights into developmental differences in Treg biology across the human lifespan and demonstrate unique functional properties of early life Tregs.

2024-06-24 | GSE262622 | GEO

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