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6 results on '"Firsching, T.C."'

1. IGF1R Plays a Protective Role in Pneumococcal Pneumonia

Author

Felten, M., primary, Teixeira Alves, L.-G., additional, Letsiou, E., additional, Alfaro Arnedo, E., additional, Piñeiro-Hermida, S., additional, López, I.P., additional, Dietert, K., additional, Firsching, T.C., additional, Gruber, A.D., additional, Fatykova, D., additional, Hocke, A.C., additional, Lingscheid, T., additional, Lienau, J., additional, Pichel, J.G., additional, and Witzenrath, M., additional

Published
2024
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2. Increased Susceptibility to Pseudomonas Aeruginosa Pneumonia in Overventilated Lungs Is Caused by Airspace Acidification Via NHE1

Author

Felten, M., primary, Chunjiang, T., additional, Ferencik, S., additional, Li, J., additional, Letsiou, E., additional, Lienau, J., additional, Mueller-Redetzky, H.C., additional, Hocke, A.C., additional, Firsching, T.C., additional, Gruber, A.D., additional, Krishnamoorthy, G., additional, Ochs, M., additional, Brandenberger, C., additional, Zhang, Q., additional, Kuebler, W.M., additional, and Witzenrath, M., additional

Published
2024
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5. Virus-induced senescence is driver and therapeutic target in COVID-19

Author

Lee, S., Yu, Y., Trimpert, J., Benthani, F., Mairhofer, M., Richter-Pechanska, P., Wyler, E., Belenki, D., Kaltenbrunner, S., Pammer, M., Kausche, L., Firsching, T.C., Dietert, K., Schotsaert, M., Martínez-Romero, C., Singh, G., Kunz, S., Niemeyer, D., Ghanem, R., Salzer, H.J.F., Paar, C., Mülleder, M., Uccellini, M., Michaelis, E.G., Khan, A., Lau, A., Schönlein, M., Habringer, A., Tomasits, J., Adler, J.M., Kimeswenger, S., Gruber, A.D., Hoetzenecker, W., Steinkellner, H., Purfuerst, B., Motz, R., Di Pierro, F., Lamprecht, B., Osterrieder, N., Landthaler, M., Drosten, C., García-Sastre, A., Langer, R., Ralser, M., Eils, R., Reimann, M., Fan, D.N.Y., and Schmitt, C.A.

Subjects
Cancer Research, Technology Platforms
Abstract

Derailed cytokine and immune cell networks account for organ damage and clinical severity of COVID-19. Here we show that SARS-CoV-2, like other viruses, evokes cellular senescence as a primary stress response in infected cells. Virus-induced senescence (VIS) is indistinguishable from other forms of cellular senescence and accompanied by a senescence-associated secretory phenotype (SASP), composed of pro-inflammatory cytokines, extracellular matrix-active factors and pro-coagulatory mediators. COVID-19 patients displayed markers of senescence in their airway mucosa in situ and elevated serum levels of SASP factors. Mirroring COVID-19 hallmark features such as macrophage and neutrophil infiltration, endothelial damage and widespread thrombosis in affected lung tissue in vitro assays demonstrated macrophage activation with SASP-reminiscent secretion, complement lysis and SASP-amplifying secondary senescence of endothelial cells, neutrophil extracellular trap (NET) formation as well as activation of platelets and the clotting cascade in response to supernatant of VIS cells, including SARS-CoV-2-induced senescence. Senolytics such as Navitoclax and Dasatinib/Quercetin selectively eliminated VIS cells, mitigated COVID-19-reminiscent lung disease and reduced inflammation in SARS-CoV-2-driven hamster and mouse models. Our findings mark VIS as pathogenic trigger of COVID-19-related cytokine escalation and organ damage, and suggest senolytic targeting of virus-infected cells as a novel treatment option against SARS-CoV-2 and perhaps other viral infections.

Published
2021

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