IL-31 signaling in pulmonary fibrosis

Pulmonary fibrosis (PF) is associated with many chronic lung diseases including Systemic sclerosis (SSc), Idiopathic Pulmonary Fibrosis (IPF) and Cystic Fibrosis (CF) which are characterized by the progressive accumulation of mesenchymal cells and formation of scar tissue. Th2 T cell-derived cytokines including IL-4 and IL-13 have been shown to contribute to inflammation and fibrotic remodeling in multiple tissues. Interleukin-31 (IL-31) is a newly identified cytokine that is predominantly produced by CD4 Th2 T cells, but its signaling receptor IL-31RA is primarily expressed by non-hematopoietic cells. However, the potential role of the IL-31-IL31RA axis in pulmonary inflammation and fibrosis has remained largely unknown. To determine the role of IL-31 signaling in pulmonary fibrosis, wildtype, and IL-31RA knockout mice were treated with bleomycin and measured changes in total lung transcripts using RNA-seq. The total lung transcriptome analysis showed a significant reduction in fibrosis-associated gene transcripts including extracellular matrix and epithelial cell-associated gene networks.

肺纤维化（Pulmonary fibrosis, PF）与多种慢性肺部疾病相关，包括系统性硬化症（Systemic sclerosis, SSc）、特发性肺纤维化（Idiopathic Pulmonary Fibrosis, IPF）及囊性纤维化（Cystic Fibrosis, CF），此类疾病以间质细胞进行性蓄积及瘢痕组织形成为典型特征。已有研究证实，Th2 T细胞来源的细胞因子（如白介素4、白介素13）可介导多组织的炎症反应与纤维化重塑。白介素31（Interleukin-31, IL-31）是新近发现的细胞因子，主要由CD4+ Th2 T细胞产生，但其信号受体IL-31RA主要表达于非造血细胞。然而，IL-31-IL31RA轴在肺部炎症与纤维化中的潜在作用仍未得到充分阐明。为明确IL-31信号通路在肺纤维化中的作用，本研究对野生型小鼠与IL-31RA基因敲除小鼠予以博莱霉素造模，并通过RNA测序（RNA-seq）检测全肺转录本的表达变化。全肺转录组分析结果显示，包括细胞外基质与上皮细胞相关基因网络在内的纤维化相关基因转录本水平显著降低。

搜集汇总

背景与挑战

背景概述

该数据集是一个关于IL-31信号在肺纤维化中作用的RNA测序研究，发布于2022年，包含16个小鼠肺组织样本。研究通过比较野生型和IL-31RA基因敲除小鼠在博来霉素处理后的转录组变化，发现IL-31信号通路缺失会显著减少纤维化相关基因的表达，为理解肺纤维化机制提供了关键数据。