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Dysregulated Innate and Adaptive Immune Responses Discriminate Disease Severity in COVID-19 #MMPMID33524124
Janssen NAF; Grondman I; de Nooijer AH; Boahen CK; Koeken VACM; Matzaraki V; Kumar V; He X; Kox M; Koenen HJPM; Smeets RL; Joosten I; Bruggemann RJM; Kouijzer IJE; van der Hoeven HG; Schouten JA; Frenzel T; Reijers MHE; Hoefsloot W; Dofferhoff ASM; van Apeldoorn MJ; Blaauw MJT; Veerman K; Maas C; Schoneveld AH; Hoefer IE; Derde LPG; van Deuren M; van der Meer JWM; van Crevel R; Giamarellos-Bourboulis EJ; Joosten LAB; van den Heuvel MM; Hoogerwerf J; de Mast Q; Pickkers P; Netea MG; van de Veerdonk FL
J Infect Dis 2021[Apr]; 223 (8): 1322-1333 PMID33524124show ga
The clinical spectrum of COVID-19 varies and the differences in host response characterizing this variation have not been fully elucidated. COVID-19 disease severity correlates with an excessive proinflammatory immune response and profound lymphopenia. Inflammatory responses according to disease severity were explored by plasma cytokine measurements and proteomics analysis in 147 COVID-19 patients. Furthermore, peripheral blood mononuclear cell cytokine production assays and whole blood flow cytometry were performed. Results confirm a hyperinflammatory innate immune state, while highlighting hepatocyte growth factor and stem cell factor as potential biomarkers for disease severity. Clustering analysis revealed no specific inflammatory endotypes in COVID-19 patients. Functional assays revealed abrogated adaptive cytokine production (interferon-gamma, interleukin-17, and interleukin-22) and prominent T-cell exhaustion in critically ill patients, whereas innate immune responses were intact or hyperresponsive. Collectively, this extensive analysis provides a comprehensive insight into the pathobiology of severe to critical COVID-19 and highlights potential biomarkers of disease severity.
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J+Infect+Dis 2021 ; 223 (8): 1322-1333
