tetano
Editor, Senior Moderator
PLoS Pathog. 2020 Feb 26;16(2):e1008334. doi: 10.1371/journal.ppat.1008334. [Epub ahead of print] [h=1]Two waves of pro-inflammatory factors are released during the influenza A virus (IAV)-driven pulmonary immunopathogenesis.[/h]
Zhang J[SUP]1,[/SUP][SUP]2[/SUP], Liu J[SUP]1[/SUP], Yuan Y[SUP]1[/SUP], Huang F[SUP]3[/SUP], Ma R[SUP]1[/SUP], Luo B[SUP]1[/SUP], Xi Z[SUP]4[/SUP], Pan T[SUP]1,[/SUP][SUP]5[/SUP], Liu B[SUP]1[/SUP], Zhang Y[SUP]1[/SUP], Zhang X[SUP]1[/SUP], Luo Y[SUP]1[/SUP], Wang J[SUP]6[/SUP], Zhao M[SUP]6[/SUP], Lu G[SUP]3[/SUP], Deng K[SUP]1[/SUP], Zhang H[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus (IAV) infection is a complicated process. After IAVs spread to the lung, extensive pro-inflammatory cytokines and chemokines are released, which largely determine the outcome of infection. Using a single-cell RNA sequencing (scRNA-seq) assay, we systematically and sequentially analyzed the transcriptome of more than 16,000 immune cells in the pulmonary tissue of infected mice, and demonstrated that two waves of pro-inflammatory factors were released. A group of IAV-infected PD-L1+ neutrophils were the major contributor to the first wave at an earlier stage (day 1-3 post infection). Notably, at a later stage (day 7 post infection) when IAV was hardly detected in the immune cells, a group of platelet factor 4-positive (Pf4+)-macrophages generated another wave of pro-inflammatory factors, which were probably the precursors of alveolar macrophages (AMs). Furthermore, single-cell signaling map identified inter-lineage crosstalk between different clusters and helped better understand the signature of PD-L1+ neutrophils and Pf4+-macrophages. Our data characteristically clarified the infiltrated immune cells and their production of pro-inflammatory factors during the immunopathogenesis development, and deciphered the important mechanisms underlying IAV-driven inflammatory reactions in the lung.
PMID: 32101596 DOI: 10.1371/journal.ppat.1008334
Zhang J[SUP]1,[/SUP][SUP]2[/SUP], Liu J[SUP]1[/SUP], Yuan Y[SUP]1[/SUP], Huang F[SUP]3[/SUP], Ma R[SUP]1[/SUP], Luo B[SUP]1[/SUP], Xi Z[SUP]4[/SUP], Pan T[SUP]1,[/SUP][SUP]5[/SUP], Liu B[SUP]1[/SUP], Zhang Y[SUP]1[/SUP], Zhang X[SUP]1[/SUP], Luo Y[SUP]1[/SUP], Wang J[SUP]6[/SUP], Zhao M[SUP]6[/SUP], Lu G[SUP]3[/SUP], Deng K[SUP]1[/SUP], Zhang H[SUP]1,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus (IAV) infection is a complicated process. After IAVs spread to the lung, extensive pro-inflammatory cytokines and chemokines are released, which largely determine the outcome of infection. Using a single-cell RNA sequencing (scRNA-seq) assay, we systematically and sequentially analyzed the transcriptome of more than 16,000 immune cells in the pulmonary tissue of infected mice, and demonstrated that two waves of pro-inflammatory factors were released. A group of IAV-infected PD-L1+ neutrophils were the major contributor to the first wave at an earlier stage (day 1-3 post infection). Notably, at a later stage (day 7 post infection) when IAV was hardly detected in the immune cells, a group of platelet factor 4-positive (Pf4+)-macrophages generated another wave of pro-inflammatory factors, which were probably the precursors of alveolar macrophages (AMs). Furthermore, single-cell signaling map identified inter-lineage crosstalk between different clusters and helped better understand the signature of PD-L1+ neutrophils and Pf4+-macrophages. Our data characteristically clarified the infiltrated immune cells and their production of pro-inflammatory factors during the immunopathogenesis development, and deciphered the important mechanisms underlying IAV-driven inflammatory reactions in the lung.
PMID: 32101596 DOI: 10.1371/journal.ppat.1008334