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1. Hypoxia shapes the immune landscape in lung injury and promotes the persistence of inflammation

Author

Mirchandani, Ananda S., Jenkins, Stephen J., Bain, Calum C., Sanchez-Garcia, Manuel A., Lawson, Hannah, Coelho, Patricia, Murphy, Fiona, Griffith, David M., Zhang, Ailiang, Morrison, Tyler, Ly, Tony, Arienti, Simone, Sadiku, Pranvera, Watts, Emily R., Dickinson, Rebecca. S., Reyes, Leila, Cooper, George, Clark, Sarah, Lewis, David, Kelly, Van, Spanos, Christos, Musgrave, Kathryn M., Delaney, Liam, Harper, Isla, Scott, Jonathan, Parkinson, Nicholas J., Rostron, Anthony J., Baillie, J. Kenneth, Clohisey, Sara, Pridans, Clare, Campana, Lara, Lewis, Philip Starkey, Simpson, A. John, Dockrell, David H., Schwarze, Jürgen, Hirani, Nikhil, Ratcliffe, Peter J., Pugh, Christopher W., Kranc, Kamil, Forbes, Stuart J., Whyte, Moira K. B., and Walmsley, Sarah R.

Published
2022
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2. Author Correction: Hypoxia shapes the immune landscape in lung injury and promotes the persistence of inflammation

Author

Mirchandani, Ananda S., Jenkins, Stephen J., Bain, Calum C., Sanchez-Garcia, Manuel A., Lawson, Hannah, Coelho, Patricia, Murphy, Fiona, Griffith, David M., Zhang, Ailiang, Morrison, Tyler, Ly, Tony, Arienti, Simone, Sadiku, Pranvera, Watts, Emily R., Dickinson, Rebecca. S., Reyes, Leila, Cooper, George, Clark, Sarah, Lewis, David, Kelly, Van, Spanos, Christos, Musgrave, Kathryn M., Delaney, Liam, Harper, Isla, Scott, Jonathan, Parkinson, Nicholas J., Rostron, Anthony J., Baillie, J. Kenneth, Clohisey, Sara, Pridans, Clare, Campana, Lara, Lewis, Philip Starkey, Simpson, A. John, Dockrell, David H., Schwarze, Jürgen, Hirani, Nikhil, Ratcliffe, Peter J., Pugh, Christopher W., Kranc, Kamil, Forbes, Stuart J., Whyte, Moira K. B., and Walmsley, Sarah R.

Published
2022
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4. Hypoxia shapes the immune landscape in lung injury promoting inflammation persistence

Author

Mirchandani, Ananda S, primary, Jenkins, Stephen J, additional, Bain, Calum C, additional, Lawson, Hannah, additional, Coelho, Patricia, additional, Murphy, Fiona, additional, Griffith, David, additional, Zhang, Ailiang, additional, Sanchez-Garcia, Manuel A, additional, Reyes, Leila, additional, Morrison, Tyler, additional, Arienti, Simone, additional, Sadiku, Pranvera, additional, Watts, Emily, additional, Dickinson, Rebecca, additional, Clark, Sarah, additional, Ly, Tony, additional, Lewis, David, additional, Kelly, Van, additional, Spanos, Christos, additional, Musgrave, Kathyrn, additional, Delaney, Liam, additional, Harper, Isla, additional, Scott, Jonathan, additional, Parkinson, Nicholas, additional, Rostron, Anthony, additional, Baillie, J Kenneth, additional, Clohisey, Sara Mary Rose, additional, Pridans, Clare, additional, Campana, Lara, additional, Starkey, Philip, additional, Simpson, A John, additional, Dockrell, David, additional, Schwarze, Jurgen, additional, Hirani, Nikhil, additional, Ratcliffe, Peter, additional, Pugh, Christopher, additional, Kranc, Kamil, additional, Forbes, Stuart, additional, Whyte, Moira, additional, and Walmsley, Sarah, additional

Published
2022
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5. A type I IFN, prothrombotic hyperinflammatory neutrophil signature is distinct for COVID-19 ARDS­­­

Author

Reyes, Leila, Sanchez Garcia, Manuel Alejandro, Morrison, Tyler, Howden, Andrew J M, Watts, Emily R, Arienti, Simone, Sadiku, Pranvera, Coelho, Patricia, Mirchandani, Ananda S, Zhang, Ailiang, Hope, David, Clark , Sarah K, Singleton, Jo, Johnston, Shonna, Grecian, Rob, Poon, Azin S., McNamara, Sarah, Harper, Isla, Fourman, Max Head, Brenes, Alejandro J, Pathak, Shalini, Lloyd, Amy, Rodriguez Blanco, Gio, von Kriegsheim, Alexander, Ghesquiere, Bart, Vermaelen, Wesley, Cologna, Camilla T, Dhaliwal, Kevin, Hirani, Nik, Dockrell, David H, Whyte, Moira K B, Griffith, David M, Cantrell, Doreen, and Walmsley, Sarah R

Abstract

Background: Acute respiratory distress syndrome (ARDS) is a severe critical condition with a high mortality that is currently in focus given that it is associated with mortality caused by coronavirus disease 2019 (COVID-19). Neutrophils play a key role in the lung injury characteristic of non-COVID-19 ARDS and there is also accumulating evidence of neutrophil mediated lung injury in patients who succumb to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).Methods: We undertook a functional proteomic and metabolomic survey of circulating neutrophil populations, comparing patients with COVID-19 ARDS and non-COVID-19 ARDS to understand the molecular basis of neutrophil dysregulation.Results: Expansion of the circulating neutrophil compartment and the presence of activated low and normal density mature and immature neutrophil populations occurs in ARDS, irrespective of cause. Release of neutrophil granule proteins, neutrophil activation of the clotting cascade and upregulation of the Mac-1 platelet binding complex with formation of neutrophil platelet aggregates is exaggerated in COVID-19 ARDS. Importantly, activation of components of the neutrophil type I interferon responses is seen in ARDS following infection with SARS-CoV-2, with associated rewiring of neutrophil metabolism, and the upregulation of antigen processing and presentation. Whilst dexamethasone treatment constricts the immature low density neutrophil population, it does not impact upon prothrombotic hyperinflammatory neutrophil signatures.Conclusions: Given the crucial role of neutrophils in ARDS and the evidence of a disordered myeloid response observed in COVID-19 patients, this work maps the molecular basis for neutrophil reprogramming in the distinct clinical entities of COVID-19 and non-COVID-19 ARDS.

Published
2021
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6. ­­­­­­­A type I IFN, prothrombotic hyperinflammatory neutrophil signature is distinct for COVID-19 ARDS­­­

Author

Reyes, Leila, primary, A. Sanchez-Garcia, Manuel, additional, Morrison, Tyler, additional, Howden, Andy J. M., additional, Watts, Emily R., additional, Arienti, Simone, additional, Sadiku, Pranvera, additional, Coelho, Patricia, additional, Mirchandani, Ananda S., additional, Zhang, Ailiang, additional, Hope, David, additional, Clark, Sarah K., additional, Singleton, Jo, additional, Johnston, Shonna, additional, Grecian, Robert, additional, Poon, Azin, additional, McNamara, Sarah, additional, Harper, Isla, additional, Fourman, Max Head, additional, Brenes, Alejandro J., additional, Pathak, Shalini, additional, Lloyd, Amy, additional, Blanco, Giovanny Rodriguez, additional, von Kriegsheim, Alex, additional, Ghesquiere, Bart, additional, Vermaelen, Wesley, additional, Cologna, Camila T., additional, Dhaliwal, Kevin, additional, Hirani, Nik, additional, Dockrell, David H., additional, Whyte, Moira K. B., additional, Griffith, David, additional, Cantrell, Doreen A., additional, and Walmsley, Sarah R., additional

Published
2021
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7. Proteomics identifies a type I IFN, prothrombotic hyperinflammatory circulating COVID-19 neutrophil signature distinct from non-COVID-19 ARDS

Author

Reyes, Leila, primary, Sanchez-Garcia, Manuel A., additional, Morrison, Tyler, additional, Howden, Andrew J.M., additional, Watts, Emily R., additional, Arienti, Simone, additional, Sadiku, Pranvera, additional, Coelho, Patricia, additional, Mirchandani, Ananda S, additional, Hope, David, additional, Clark, Sarah K., additional, Singleton, Jo, additional, Johnston, Shonna, additional, Grecian, Robert, additional, Poon, Azin, additional, Mcnamara, Sarah, additional, Harper, Isla, additional, Fourman, Max Head, additional, Brenes, Alejandro J., additional, Pathak, Shalini, additional, Lloyd, Amy, additional, Blanco, Gio Rodriguez, additional, Kriegsheim, Alex von, additional, Ghesquiere, Bart, additional, Vermaelen, Wesley, additional, Cologna, Camila T., additional, Dhaliwal, Kevin, additional, Hirani, Nik, additional, Dockrell, David, additional, Whyte, Moira K., additional, Griffith, David, additional, Cantrell, Doreen A., additional, and Walmsley, Sarah R., additional

Published
2020
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