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Gene signature profiles in bronchial tissues from severe asthma patients treated with bronchial thermoplasty

ABSTRACT: Bronchial thermoplasty (BT) is an endoscopic therapy employed for the treatment of refractory asthma. However, no predictive factors are available that determine the effectiveness of BT in treating asthma patients. The present study aimed to comprehensively analyze RNA samples from the airway bronchial tissues of 8 patients with severe asthma treated by BT, and to characterize each patient as a BT responder or non-responder. Total 24 RNA samples (three per patient prior to BT1 [baseline], prior to BT2 [after 1st time treatment], and prior to BT3 [after 2nd time treatment]) were obtained. There were 975 differentially expressed (DE) genes in the bronchial tissues of 8 patients between prior to BT1 (baseline) and prior to BT2 (after 1st time treatment), with significant differences (FDR-adjusted P<0.05). Subjects with an Asthma Quality of Life Questionnaire score change of >0.5 for a period of 12 months were considered BT responders. Non-responders exhibited a score change of <0.5 for 12 months. Transcriptome analysis at baseline identified 67 genes that were differentially expressed between responders and non-responders, including SLPI, MMP3, and MUC19 which were upregulated in responders.

ORGANISM(S): Homo sapiens

PROVIDER: GSE159091 | GEO | 2021/06/22

REPOSITORIES: GEO

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Project description:In the present study, we studied chronic HCV patients who responded to IFN-based therapy as evidenced by absence of HCV RNA at the end of treatment, and focused on two issues that have not received much attention. Firstly, we evaluated whether specific genes or gene expression patterns in blood were able to distinguish responder patients with a viral relapse from responder patients who remained virus-negative after cessation of treatment. We found that chronic HCV patients who were sustained responders and relapsers to IFN-based therapy showed comparable baseline clinical parameters and immune composition in blood. However, at baseline, the gene expression profiles of a set of 18 genes predicted treatment outcome with an accuracy of 94%. Secondly, we examined whether patients with successful therapy-induced clearance of HCV still exhibited gene expression patterns characteristic for HCV, or whether normalization of their transcriptome was observed. We observed that the relatively high expression of IFN-stimulated genes (ISG) in chronic HCV patients prior to therapy was reduced after successful IFN-based antiviral therapy (at 24 weeks follow-up). These ISG included CXCL10, OAS1, IFI6, DDX60, TRIM5 and STAT1. In addition, 1428 differentially expressed non-ISG genes were identified in paired pre- and post-treatment samples from sustained responders, which included genes involved in TGF-β signaling, apoptosis, autophagy, and nucleic acid and protein metabolism. Interestingly, 1424 genes were identified with altered expression in responder patients after viral eradication in comparison to normal expression levels in healthy individuals. Additionally, aberrant expression of a subset of these genes, including IL-32, IL-16, CCND3 and RASSF1, was also observed at baseline. Our findings indicate that successful antiviral therapy of chronic HCV patients does not lead to normalization of their blood transcriptional signature. The altered transcriptional activity may reflect HCV-induced liver damage in previously infected individuals. A genome-wide gene expression analysis was performed on a blood cohort of 59 chronic HCV patients and 20 healthy controls. The expression profiles of patients who responded to IFN-based therapy, who developed a viral relapse were compared respectively to the profiles of healthy controls. Pre- and post-treatment expression profiles of same responders were compared as well.

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Gene signature profiles in bronchial tissues from severe asthma patients treated with bronchial thermoplasty

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