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ABSTRACT: Nontuberculous mycobacteria disease in cystic fibrosis

PROVIDER: PRJNA594304 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10608200_1.fastq.gz	Fastqsanger.gz
	SRR10608200_2.fastq.gz	Fastqsanger.gz
	SRR10608300_1.fastq.gz	Fastqsanger.gz
	SRR10608300_2.fastq.gz	Fastqsanger.gz
	SRR10608400_1.fastq.gz	Fastqsanger.gz

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Whole blood gene expression to predict susceptibility to nontuberculous mycobacterial pulmonary disease in adults with cystic fibrosis

Project description:Background: Patients with cystic fibrosis (CF) have an elevated lifetime risk of infection and disease caused by nontuberculous mycobacteria (NTM). Currently, there is no method to predict whether patients with cystic fibrosis will develop disease related to non-tuberculous mycobacteria. In non cystic fibrosis populations, several genetic susceptibility factors have been described. In this study, we examined whether patients with cystic fibrosis demonstrate a similar pattern of genetic susceptibility and explored host immune-related biomarkers predictive of NTM pulmonary disease (NTM-PD). Methods: We evaluated whole blood gene expression using bulk RNA-seq in a cohort of CF patients at the time of first isolation of NTM. Differential gene expression was compared in patients who did (n = 12) vs. did not (n= 30) develop NTM-PD following first NTM growth. Results: No differences in demographics or composition of white blood cell sample populations at the time of sample collection were identified between groups. There were no significant differences in the expression of genes previously reported to confer susceptibility to NTM-PD in non-CF populations. However, CF patients who went on to develop NTM-PD had higher expression of genes involved in the interferon ( and ), tumor necrosis factor, and IL6 STAT3 JAK pathways. Conclusion: Patients with CF who develop NTM-PD have increased expression of genes involved in innate immunity, in contrast to non-CF populations where these responses seem to be suppressed.

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Project description:Rationale: Nontuberculous mycobacteria (NTM) infection can promote progressive lung function decline and damage, a condition known as NTM Pulmonary Disease (NTM-PD). Mycobacterium abscessus complex (MABSC) is a common cause of infections in people with cystic fibrosis (pwCF). Here, we performed the first single-cell transcriptome characterization of circulating cellular transcripts in pwCF at risk of MABSC infections. Objectives: To define the circulating immune transcriptional profiles of pwCF with MABSC colonization or MABSC pulmonary disease. Methods: We isolated peripheral blood mononuclear cell (PBMCs) and blood plasma of 12 pwCF including those displayed MABSC colonization or pulmonary disease and those with no history of NTM detection as control group. To identify immune signatures, we performed single cell (sc)RNA-sequencing and Luminex assay and validate our findings publicpublicly available datasets. Measurements and Main Results: We determined 10 cells populations annotated according to the expression levels and performed differentially expressed genes analysis among the three groups in each cellular population. We found out that pwCF with active MABSC pulmonary disease showed i) a set of transcripts specifically upregulated in CD14+ and CD16+ monocytes, ii) a downregulation of expression profiles related to NK and CD8 T cellular clusters, iii) the identified CD14+ monocytes characterized by IFNs signalling and pro-inflammatory pathways. In addition, we confirmed the highest CXCL10 levels in pwCF with pulmonary disease. Moreover, we validated our findings in a second publicpublicly available datasets from a cohort of pwCF infected by MABSC. Conclusions: Overall, we applyedapplied scRNAseq technologies to circulating blood cells and defined that circulating hyperinflammatory monocyte responses are associated to MABSC pulmonary disease in pwCF.

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Project description:We have compared gene expression in human nasal brushing cells from 19 cystic fibrosis (CF) patients and 19 healthy controls using a 5.2K cDNA microarray. Our aim is to identify new disease biomarkers for the Cystic Fibrosis Gene Therapy Consortium. These markers will be used to report more effectively on the response to the administration of gene therapy in vivo. Cystic Fibrosis is a recessive genetic disease caused by mutations in the cystic fibrosis conductance regulator (CFTR) gene which encodes a chloride ion channel. The most common mutation is the ∆F508 mutation, present on 70% of CF chromosomes in Caucasian populations. The disease affects many organs in the body such as the pancreas, liver, sweat glands, small intestine and reproductive tracts but is most commonly associated with progressive, inflammatory lung disease. The current average life expectancy of CF patients is 35 years. Gene therapy is being developed as a treatment for CF airway disease, however, means of measuring the efficiency and efficacy of gene therapy in vivo are lacking. This is mainly due to the difficulty in measuring the chloride conductance of CFTR in cells and tissues. Furthermore, clinical assays for measuring improvements in lung function are insensitive. Surrogate markers of inflammation and CFTR function will therefore be important for the effective assessment of gene therapy in vivo. We have analysed gene expression in human nasal epithelium as this is considered an accessible surrogate for the conducting airways where disease manifests in the majority of patients. Additionally, this tissue will be sampled in clinical trials.

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