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RNA-seq of CD11b DCs from mice with established pulmonary fibrosis

ABSTRACT: RNA-seq of CD11b DCs from mice with established pulmonary fibrosis

PROVIDER: PRJNA477779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7419690.fastq.gz	Fastqsanger.gz
	SRR7419681.fastq.gz	Fastqsanger.gz
	SRR7419691.fastq.gz	Fastqsanger.gz
	SRR7419682.fastq.gz	Fastqsanger.gz
	SRR7419692.fastq.gz	Fastqsanger.gz

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Project description:Background: The transition from normal lung anatomy to minimal and established fibrosis is a well-established feature of the pathology of idiopathic pulmonary fibrosis (IPF). The purpose of this report is to examine the molecular and cellular mechanisms associated with this transition. Methods: Pre-operative thoracic MDCT scans of patients with severe IPF (n=9) treated by lung transplantation were used to identify regions of minimal (n=27) and established fibrosis (n=27). Micro-CT, quantitative histology and next-generation sequencing (RNAseq) were used to compare 24 samples from donor controls to minimal and established fibrosis samples. Findings: The present results confirmed an earlier report showing that the transition from normal lung anatomy to minimal and established fibrosis was associated with a reduction in the numbers of terminal bronchioles. In addition, this study substantially extended those observations by showing the activation of TGFBI, TLRs, NFÃŽÂºB, TGFÃŽÂ² pathways, and T cell co-stimulatory genes, as well as the down-regulation of inhibitory immune checkpoint genes in IPF affected lung tissue. The expression patterns of these genes indicated activation of a field immune response, which is further supported by the increased infiltration of inflammatory immune cells dominated by lymphocytes that are capable of forming the non-encapsulated lymphoid follicles. Fibrosis pathways, mucin secretion, surfactant, and cytokine storm-related genes also participate in the transitions from normal lung anatomy to minimal and established fibrosis. Interpretation: The transition from normal lung anatomy to minimal and established fibrosis is associated with the up-regulation of TGFBI, TLRs, NFÃŽÂºB, TGFÃŽÂ² pathways, cytokine storm-related genes, and the down-regulation of inhibitory immune checkpoint, surfactant genes as well as the increased infiltration of CD4, CD8, B cell lymphocytes, and macrophages. These molecular and cellular events all contribute to the pathogenesis of IPF.

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RNA-seq of CD11b DCs from mice with established pulmonary fibrosis

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