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Contrasting gene expression patterns associated with high and low rhinovirus stimulated IFN-α production

ABSTRACT: Contrasting gene expression patterns associated with high and low rhinovirus stimulated IFN-α production

PROVIDER: PRJNA700069 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13645400_1.fastq.gz	Fastqsanger.gz
	SRR13645400_2.fastq.gz	Fastqsanger.gz
	SRR13645500_1.fastq.gz	Fastqsanger.gz
	SRR13645500_2.fastq.gz	Fastqsanger.gz
	SRR13645401_1.fastq.gz	Fastqsanger.gz

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Contrasting gene expression patterns associated with high and low rhinovirus stimulated IFN-α production

Project description:Introduction: Viral respiratory infections cause considerable morbidity and economic loss. While rhinoviruses (RV) typically cause little more than the common cold, they can produce severe infections and disease exacerbations in susceptible individuals, including those with chronic lung diseases. Variations in the regulation of key antiviral cytokines, particularly type I interferon (IFN-α and IFN-b), may contribute to RV susceptibility, but are not well understood. Method: Whole genome transcription patterns were assessed in samples from 74 individuals demonstrating high or low IFN-α production following RV stimulation in vitro. Results: In unstimulated samples (baseline) the high IFN-α producer group showed higher expression of genes associated with plasmacytoid dendritic cells, the complement system, B-cell chemokines, immune regulation, macrophages, and vitamin D activation and lower expression of genes linked to haemoglobin and haem biosynthesis, wound healing, stress response and pro-inflammatory genes than the low IFN-α producer group. After RV stimulation, the high IFN-α producer group showed more intense upregulation of diverse immune function genes including IFNs and greater downregulation of genes linked to structural and extra-cellular matrix functions than the low IFN-α producer group. Patterns of antibacterial gene expression varied between groups. Healthy people and those with asthma generally showed similar gene expression patterns. These findings highlight multiple biological pathways whose expression patterns differ substantially between high and low IFN-α producers. These differences likely contribute to variations in anti-RV immunity and immunopathology between individuals.

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Project description:Human rhinovirus (HRV) infection is a major cause of asthma exacerbations, which appears to be linked to a defective innate immune response to infection. Although the type I interferons (IFN-α and IFN-β) have a critical role in protecting against most viral infections, the cells responsible for IFN production in response to HRV and the relative importance of pattern recognition receptors located in endosomes has not been fully elucidated. In the current study we demonstrate that, using intracellular flow cytometry, >90% of the IFN-α-producing cells in human blood mononuclear cells following HRV16 exposure are plasmacytoid dendritic cells, whereas monocytes and myeloid dendritic cells contribute only 10% and <1%, respectively, of the IFN-α production. Bafilomycin and chloroquine, agents that inhibit the function of endosomal toll-like receptors (TLRs), significantly reduced the capacity of TLR3-, TLR7- and TLR-9-stimulated cells to produce IFN-α and the IFN-induced chemokine CXCL10 (IP-10). In contrast, only bafilomycin (but not chloroquine) effectively suppressed HRV16-stimulated IFN-α and IP-10 production, whereas neither bafilomycin or chloroquine inhibited HRV16-stimulated interleukin-6 release. Attempts to block IFN-α production with commercially available TLR-specific oligonucleotides were unsuccessful due to major 'off-target' effects. These findings suggest that among circulating haemopoietic cells, plasmacytoid dendritic cells and TLRs located within endosomes are critical for inducing efficient IFN-I production in response to HRVs.

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