Author: Schimke, Lena F.; Marques, Alexandre H.C.; Baiocchi, Gabriela Crispim; de Souza Prado, Caroline Aliane; Fonseca, Dennyson Leandro M.; Freire, Paula Paccielli; Plaça, Desirée Rodrigues; Filgueiras, Igor Salerno; Salgado, Ranieri Coelho; Jansen-Marques, Gabriel; Oliveira, Antonio Edson Rocha; Peron, Jean Pierre Schatzmann; Barbuto, José Alexandre Marzagão; Camara, Niels Olsen Saraiva; Calich, Vera Lúcia Garcia; Ochs, Hans D.; Condino-Neto, Antonio; Overmyer, Katherine A.; Coon, Joshua J.; Balnis, Joseph; Jaitovich, Ariel; Schulte-Schrepping, Jonas; Ulas, Thomas; Schultze, Joachim L.; Nakaya, Helder I.; Jurisica, Igor; Cabral-Marques, Otavio
Title: Multi-layered transcriptomic analyses reveal an immunological overlap between COVID-19 and hemophagocytic lymphohistiocytosis associated with disease severity Cord-id: 2t4j7bvg Document date: 2021_8_1
ID: 2t4j7bvg
Snippet: Clinical and hyperinflammatory overlap between COVID-19 and hemophagocytic lymphohistiocytosis (HLH) has been reported. However, the underlying mechanisms are unclear. Here we show that COVID-19 and HLH have an overlap of signaling pathways and gene signatures commonly dysregulated, which were defined by investigating the transcriptomes of 1253 subjects (controls, COVID-19, and HLH patients) using microarray, bulk RNA-sequencing (RNAseq), and single-cell RNAseq (scRNAseq). COVID-19 and HLH share
Document: Clinical and hyperinflammatory overlap between COVID-19 and hemophagocytic lymphohistiocytosis (HLH) has been reported. However, the underlying mechanisms are unclear. Here we show that COVID-19 and HLH have an overlap of signaling pathways and gene signatures commonly dysregulated, which were defined by investigating the transcriptomes of 1253 subjects (controls, COVID-19, and HLH patients) using microarray, bulk RNA-sequencing (RNAseq), and single-cell RNAseq (scRNAseq). COVID-19 and HLH share pathways involved in cytokine and chemokine signaling as well as neutrophil-mediated immune responses that associate with COVID-19 severity. These genes are dysregulated at protein level across several COVID-19 studies and form an interconnected network with differentially expressed plasma proteins which converge to neutrophil hyperactivation in COVID-19 patients admitted to the intensive care unit. scRNAseq analysis indicated that these genes are specifically upregulated across different leukocyte populations, including lymphocyte subsets and immature neutrophils. Artificial intelligence modeling confirmed the strong association of these genes with COVID-19 severity. Thus, our work indicates putative therapeutic pathways for intervention.
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