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ABSTRACT: Trancriptional signatures of dexamethasone-treated sarcoidosis alveolar macrophages (AMs)

PROVIDER: PRJNA630000 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11670479_1.fastq.gz	Fastqsanger.gz
	SRR11670479_2.fastq.gz	Fastqsanger.gz
	SRR11670480_1.fastq.gz	Fastqsanger.gz
	SRR11670480_2.fastq.gz	Fastqsanger.gz
	SRR11670481_1.fastq.gz	Fastqsanger.gz

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Trancriptional signatures of dexamethasone-treated sarcoidosis alveolar macrophages (AMs)

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Project description:Pulmonary sarcoidosis is an inflammatory disease characterized by granuloma formation and heterogeneous clinical outcome. TNF is a proinflammatory cytokine contributing to granuloma formation and high levels of TNF have been shown to associate with progressive disease. Mononuclear phagocytes (MNPs) are potent producers of TNF and highly responsive to inflammation. In sarcoidosis, alveolar macrophages (AMs) have been well studied. However, MNPs also include monocytes/monocyte-derived cells and dendritic cells (DCs) that despite their central role in inflammation are poorly studied in sarcoidosis. We performed in-depth phenotypic, functional and transcriptomic analysis of MNPs subsets from blood and bronchoalveolar lavage (BAL) fluid from 108 sarcoidosis patients and 30 healthy controls.

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Project description:Alveolar macrophages (AMs) are lung resident phagocytes. They derive from fetal liver monocytes, which colonize the lung during embryonic development and give rise to fully mature AMs perinatally. We have identified TGF- signaling as an indispensible regulator during this process. To analyze the impact of TGF- on the entire transcriptome of AMs, we performed RNA-seq on AMs deficient of Tgfbr2 in CD11cCre/+ Tgfbr2fl/fl mice at P3 with Tgfbr2fl/fl littermates as a control.

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Project description:Tumor microenvironment components, including T and myeloid cells, play important roles in lung adenocarcinoma (LADC) progression and response to therapy. Here, we identify a role for Siah1a/2 ubiquitin ligases in controlling alveolar macrophage (AM) differentiation and urethane-induced LADC. Genetic ablation of Siah1a/2 in AMs enriched their immature state, coinciding with increased pro-tumorigenic and inflammatory gene signatures and abundance of Siah1a/2 substrates NRF2 and B-catenin. Urethane administration to mice enriched the population of monocytic and immature-like AMs, which were more prevalent in the lungs of mice carrying Siah1a/2-ablated macrophages. While resembling transitional profibrotic macrophages often seen in lung fibrosis, enrichment of immature AMs coincided with the development of more frequent and larger lung tumors in urethane-treated mice harboring Siah1a/2 ablated macrophages compared with controls. Gene expression signature of Siah1a/2 ablated immature-like AMs is associated with increased infiltration of CD14+ immune cells and worse survival of LADC patients. Our findings identify Siah1a/2 as gatekeepers of cancer development by controlling AM differentiation and profibrotic phenotypes contributing to carcinogen-induced lung cancer.

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