The exact immunopathophysiology of community-acquired pneumonia (CAP) caused by SARS-CoV-2 (COVID-19) remains clouded by a general lack of relevant disease controls. The scarcity of single-cell investigations in the broader population of patients with CAP renders it difficult to distinguish immune features unique to COVID-19 from the common characteristics of a dysregulated host response to pneumonia. We performed integrated single-cell transcriptomic and proteomic analyses in peripheral blood mononuclear cells from a matched cohort of eight patients with COVID-19, eight patients with CAP caused by Influenza A or other pathogens, and four non-infectious control subjects. Using this balanced, multi-omics approach, we describe shared and diverging transcriptional and phenotypic patterns—including increased levels of type I interferon-stimulated natural killer cells in COVID-19, cytotoxic CD8 T EMRA cells in both COVID-19 and influenza, and distinctive monocyte compositions between all groups—and thereby expand our understanding of the peripheral immune response in different etiologies of pneumonia.
【저자키워드】 COVID-19, Pneumonia, Human, PBMC, 【초록키워드】 SARS-CoV-2, Influenza, host response, CD8, peripheral immune response, immune, monocyte, Peripheral blood, Cohort, Characteristics, Patient, Pathogens, etiology, disease, single-cell, proteomic, community-acquired pneumonia, natural killer cell, Analysis, mononuclear cell, control subjects, type I, phenotypic, non-infectious, transcriptomic, approach, controls, feature, Cell, transcriptional, performed, lack, caused, eight, unique, dysregulated, expand, patients with COVID-19, 【제목키워드】 Influenza, immune, single-cell, community-acquired pneumonia, Analysis, feature,