Behavioural immune landscapes of inflammation

Crainiciuc, Georgiana; Palomino‐Segura, Miguel; Molina-Moreno, Miguel; Sicilia, Jon; Aragones, David G.; Li, Jackson Liang Yao; Madurga, Rodrigo; Adrover, José M.; Aroca-Crevillén, Alejandra; Martín-Salamanca, Sandra; Valle, Alfonso; Castillo, Sandra D.; Welch, Heidi; Soehnlein, Oliver; Graupera, Mariona; Sánchez-Cabo, Fátima; Zarbock, Alexander; Smithgall, Thomas E.; Pilato, Mauro Di; Mempel, Thorsten R.; Tharaux, Pierre‐Louis; González, Santiago F.; Ayuso-Sacido, Ángel; Ng, Lai Guan; Calvo, Gabriel F.; González-Díaz, Iván; Díaz-de-María, Fernando; Hidalgo, Andrés

doi:10.1038/s41586-021-04263-y

Cited by 59 publications

(32 citation statements)

References 34 publications

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“…Furthermore, our data should open new perspectives in the development of innovative immunotherapy strategies. Recently, Crainiciuc et al identify the Src kinase Fgr as a driver of the pathogenic senescent state of neutrophils, and interference with Fgr protected mice from inflammatory injury in a model of ischemia–reperfusion [ 66 ]. In addition, targeting junctional adhesion molecule-C has been reported to improve sepsis-induced acute lung injury by decreasing CXCR4 + aged neutrophils [ 67 ].…”

Section: Discussionmentioning

confidence: 99%

Impairment of neutrophil functions and homeostasis in COVID-19 patients: association with disease severity

et al. 2022

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Background A dysregulated immune response is emerging as a key feature of critical illness in COVID-19. Neutrophils are key components of early innate immunity that, if not tightly regulated, contribute to uncontrolled systemic inflammation. We sought to decipher the role of neutrophil phenotypes, functions, and homeostasis in COVID-19 disease severity and outcome. Methods By using flow cytometry, this longitudinal study compares peripheral whole-blood neutrophils from 90 COVID-19 ICU patients with those of 22 SARS-CoV-2-negative patients hospitalized for severe community-acquired pneumonia (CAP) and 38 healthy controls. We also assessed correlations between these phenotypic and functional indicators and markers of endothelial damage as well as disease severity. Results At ICU admission, the circulating neutrophils of the COVID-19 patients showed continuous basal hyperactivation not seen in CAP patients, associated with higher circulating levels of soluble E- and P-selectin, which reflect platelet and endothelial activation. Furthermore, COVID-19 patients had expanded aged-angiogenic and reverse transmigrated neutrophil subsets—both involved in endothelial dysfunction and vascular inflammation. Simultaneously, COVID-19 patients had significantly lower levels of neutrophil oxidative burst in response to bacterial formyl peptide. Moreover patients dying of COVID-19 had significantly higher expansion of aged-angiogenic neutrophil subset and greater impairment of oxidative burst response than survivors. Conclusions These data suggest that neutrophil exhaustion may be involved in the pathogenesis of severe COVID-19 and identify angiogenic neutrophils as a potentially harmful subset involved in fatal outcome. Graphic Abstract

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Section: Discussionmentioning

confidence: 99%

Impairment of neutrophil functions and homeostasis in COVID-19 patients: association with disease severity

et al. 2022

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“…Endothelial cells and pericytes surrounding pulmonary blood vessels and capillary sites vasodilate, becoming more permeable, and increase expression of surface adhesion molecules to allow extravasation of peripheral immune cells from the blood. A new area of investigation, culminating in an initial 2022 study, aimed to capture the numerous and rapid cellular transitional states (e.g., motility and morphology) of individual cells during acute inflammatory responses—a task that had been, until recently, technologically limited ( Crainiciuc et al., 2022 ). Using 4D live imaging of individual leukocytes at sites of active inflammation paired with constructed behavioral landscapes, investigators were able to characterize the continuous morphokinetic and behavioral changes in single leukocytes as they adapted to local cues, tissue barriers, and acute states of inflammation.…”

Section: Innate Respiratory Response: Acute Pulmonary Inflammationmentioning

confidence: 99%

Mucosal immune responses to infection and vaccination in the respiratory tract

Mettelman

Allen²,

Thomas³

2022

Immunity

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“…Enzyme targets include cGAS ( Ablasser and Chen, 2019 ); the kinases JAK1/2 ( Hoang et al., 2021 ), ephrin-B3 ( Clark et al., 2021 ), and Fgr ( Crainiciuc et al., 2022 ); the tyrosine phosphatase SHP2 ( Paccoud et al., 2021 ); the proteases proprotein convertase subtilisin/Kexin 9 (PCSK 9) ( Patriki et al., 2022 ) and the immunoproteasome ( Ah Kioon et al., 2021 ; Kirk et al., 2021 ); the 8-oxoguanine DNA glycosylase OGG-1 ( Visnes et al., 2018 ); and the histone 3 Lys27 trimethyltransferase Ezh2 ( Zhang et al., 2018 ). Adaptor protein targets include STING ( Ablasser and Chen, 2019 ) and NRLP3 ( Wang et al., 2022 ).…”

Section: Suppressing Inflammationmentioning

confidence: 99%

Nonresolving inflammation redux

Nathan

2022

Immunity

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Behavioural immune landscapes of inflammation

Cited by 59 publications

References 34 publications

Impairment of neutrophil functions and homeostasis in COVID-19 patients: association with disease severity

Impairment of neutrophil functions and homeostasis in COVID-19 patients: association with disease severity

Mucosal immune responses to infection and vaccination in the respiratory tract

Nonresolving inflammation redux

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