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Interstitial Macrophage Phenotypes in Schistosoma-Induced Pulmonary Hypertension

GSE254338 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2024/05/08 Platform GPL24247
Summary
Schistosomiasis, a prevalent cause of pulmonary hypertension (PH) globally, triggers type 2 inflammation, with interstitial macrophages (IMs) derived from monocytes playing a crucial role. These IMs produce thrombospondin-1 (TSP-1), activating TGF-β and driving PH pathology. Two distinct IM subpopulations were identified: resident FOLR2+ IMs expressing monocyte recruitment factors, and recruited CCR2+ IMs expressing TSP-1. Upon exposure to Schistosoma, the CCR2+ subpopulation expanded. Flow cytometry and single-cell RNA sequencing confirmed these findings, revealing crosstalk between IM subpopulations. The resident FOLR2+ IMs increased expression of monocyte recruitment ligands, while the recruited CCR2+ IMs expressed elevated TSP-1, activating TGF-β and contributing to PH. This study provides insights into the complex interplay of IM subpopulations in Schistosoma-induced PH, shedding light on potential therapeutic targets for this global health concern.
Published in
Interstitial macrophage phenotypes in Schistosoma-induced pulmonary hypertension
Kumar R, Kumar S, Mickael C et al. · Frontiers in immunology 2024 · PMID 38779688 · doi:10.3389/fimmu.2024.1372957
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Direct links to NCBI, no account and no request form: the whole study as GSE254338_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1069761 and SRA study SRP486169. Searching any of these in the dataset finder brings you back here.

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