tetano
Editor, Senior Moderator
Proc Natl Acad Sci U S A
. 2023 Dec 19;120(51):e2300474120.
doi: 10.1073/pnas.2300474120. Epub 2023 Dec 15. Pleural macrophages translocate to the lung during infection to promote improved influenza outcomes
James P Stumpff 2nd[SUP] 1 [/SUP], Sang Yong Kim[SUP] 2 [/SUP], Matthew I McFadden[SUP] 3 4 [/SUP], Andrew Nishida[SUP] 5 [/SUP], Roksana Shirazi[SUP] 1 [/SUP], Yael Steuerman[SUP] 6 [/SUP], Irit Gat-Viks[SUP] 6 [/SUP], Adriana Forero[SUP] 3 4 [/SUP], Meera G Nair[SUP] 2 [/SUP], Juliet Morrison[SUP] 1 [/SUP]
Affiliations
Seasonal influenza results in 3 to 5 million cases of severe disease and 250,000 to 500,000 deaths annually. Macrophages have been implicated in both the resolution and progression of the disease, but the drivers of these outcomes are poorly understood. We probed mouse lung transcriptomic datasets using the Digital Cell Quantifier algorithm to predict immune cell subsets that correlated with mild or severe influenza A virus (IAV) infection outcomes. We identified a unique lung macrophage population that transcriptionally resembled small serosal cavity macrophages and whose presence correlated with mild disease. Until now, the study of serosal macrophage translocation in the context of viral infections has been neglected. Here, we show that pleural macrophages (PMs) migrate from the pleural cavity to the lung after infection with IAV. We found that the depletion of PMs increased morbidity and pulmonary inflammation. There were increased proinflammatory cytokines in the pleural cavity and an influx of neutrophils within the lung. Our results show that PMs are recruited to the lung during IAV infection and contribute to recovery from influenza. This study expands our knowledge of PM plasticity and identifies a source of lung macrophages independent of monocyte recruitment and local proliferation.
Keywords: influenza; macrophages; pleural cavity; tissue deconvolution; transcriptomics.
. 2023 Dec 19;120(51):e2300474120.
doi: 10.1073/pnas.2300474120. Epub 2023 Dec 15. Pleural macrophages translocate to the lung during infection to promote improved influenza outcomes
James P Stumpff 2nd[SUP] 1 [/SUP], Sang Yong Kim[SUP] 2 [/SUP], Matthew I McFadden[SUP] 3 4 [/SUP], Andrew Nishida[SUP] 5 [/SUP], Roksana Shirazi[SUP] 1 [/SUP], Yael Steuerman[SUP] 6 [/SUP], Irit Gat-Viks[SUP] 6 [/SUP], Adriana Forero[SUP] 3 4 [/SUP], Meera G Nair[SUP] 2 [/SUP], Juliet Morrison[SUP] 1 [/SUP]
Affiliations
- PMID: 38100417
- DOI: 10.1073/pnas.2300474120
Seasonal influenza results in 3 to 5 million cases of severe disease and 250,000 to 500,000 deaths annually. Macrophages have been implicated in both the resolution and progression of the disease, but the drivers of these outcomes are poorly understood. We probed mouse lung transcriptomic datasets using the Digital Cell Quantifier algorithm to predict immune cell subsets that correlated with mild or severe influenza A virus (IAV) infection outcomes. We identified a unique lung macrophage population that transcriptionally resembled small serosal cavity macrophages and whose presence correlated with mild disease. Until now, the study of serosal macrophage translocation in the context of viral infections has been neglected. Here, we show that pleural macrophages (PMs) migrate from the pleural cavity to the lung after infection with IAV. We found that the depletion of PMs increased morbidity and pulmonary inflammation. There were increased proinflammatory cytokines in the pleural cavity and an influx of neutrophils within the lung. Our results show that PMs are recruited to the lung during IAV infection and contribute to recovery from influenza. This study expands our knowledge of PM plasticity and identifies a source of lung macrophages independent of monocyte recruitment and local proliferation.
Keywords: influenza; macrophages; pleural cavity; tissue deconvolution; transcriptomics.