Metabolic stress and disease-stage specific basigin expression of peripheral blood immune cell subsets in COVID-19 patients
Siska, P. J.; Singer, K.; Klitzke, J.; Kauer, N.; Decking, S.-M.; Bruss, C.; Matos, C.; Kolodova, K.; Peuker, A.; Schoenhammer, G.; Raithel, J.; Lunz, D.; Graf, B.; Geismann, F.; Lubnow, M.; Mack, M.; Hau, P.; Bohr, C.; Burkhardt, R.; Gessner, A.; Salzberger, B.; Hanses, F.; Hitzenbichler, F.; Heudobler, D.; Lueke, F.; Pukrop, T.; Herr, W.; Wolff, D.; Poeck, H.; Brochhausen, C.; Hoffmann, P.; Rehli, M.; Kreutz, M.; Renner, K.
Show abstract
Coronavirus disease 2019 (COVID-19) is driven by dysregulated immune responses yet the role of immunometabolism in COVID-19 pathogenesis remains unclear. By investigating 47 patients with confirmed SARS-CoV-2 infection and 16 uninfected controls, we found an immunometabolic dysregulation specific for patients with progressed disease that was reversible in the recovery phase. Specifically, T cells and monocytes exhibited increased mitochondrial mass, accumulated intracellular ROS and these changes were accompanied by disrupted mitochondrial architecture. Basigin (CD147), but not established markers of T cell activation, was up-regulated on T cells from progressed COVID-19 patients and correlated with ROS accumulation, reflected in the transcriptome. During recovery, basigin and ROS decreased to match the uninfected controls. In vitro analyses confirmed the correlation and showed a down-regulation of ROS by dexamethasone treatment. Our findings provide evidence of a basigin-related and reversible immunometabolic dysregulation in COVID-19.
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