Background Analyses of blood biomarkers involved in the host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection can reveal distinct biological pathways and inform development and testing of therapeutics for COVID-19. Our objective was to evaluate host endothelial, epithelial and inflammatory biomarkers in COVID-19. Methods We prospectively enrolled 171 ICU patients, including 78 (46%) patients positive and 93 (54%) negative for SARS-CoV-2 infection from April to September, 2020. We compared 22 plasma biomarkers in blood collected within 24 h and 3 days after ICU admission. Results In critically ill COVID-19 and non-COVID-19 patients, the most common ICU admission diagnoses were respiratory failure or pneumonia, followed by sepsis and other diagnoses. Similar proportions of patients in both groups received invasive mechanical ventilation at the time of study enrollment. COVID-19 and non-COVID-19 patients had similar rates of acute respiratory distress syndrome, severe acute kidney injury, and in-hospital mortality. While concentrations of interleukin 6 and 8 were not different between groups, markers of epithelial cell injury (soluble receptor for advanced glycation end products, sRAGE) and acute phase proteins (serum amyloid A, SAA) were significantly higher in COVID-19 compared to non-COVID-19, adjusting for demographics and APACHE III scores. In contrast, angiopoietin 2:1 (Ang-2:1 ratio) and soluble tumor necrosis factor receptor 1 (sTNFR-1), markers of endothelial dysfunction and inflammation, were significantly lower in COVID-19 ( p < 0.002). Ang-2:1 ratio and SAA were associated with mortality only in non-COVID-19 patients. Conclusions These studies demonstrate that, unlike other well-studied causes of critical illness, endothelial dysfunction may not be characteristic of severe COVID-19 early after ICU admission. Pathways resulting in elaboration of acute phase proteins and inducing epithelial cell injury may be promising targets for therapeutics in COVID-19. Supplementary Information The online version contains supplementary material available at 10.1186/s13054-021-03547-z.
【저자키워드】 COVID-19, Critical illness, acute respiratory distress syndrome, Endothelial dysfunction, 【초록키워드】 SARS-CoV-2, Inflammation, Necrosis, Tumor, Respiratory distress syndrome, viral infection, Critical illness, coronavirus, Biomarker, Respiratory failure, Mortality, severe COVID-19, acute respiratory distress syndrome, Pneumonia, Therapeutics, SARS-COV-2 infection, Sepsis, Acute kidney injury, host response, severe acute respiratory syndrome Coronavirus, Endothelial dysfunction, interleukin 6, angiopoietin, Protein, interleukin, tumor necrosis factor, Viral, Critically ill, Patient, ICU admission, target, ICU Patients, targets, receptor, respiratory, characteristic, epithelial, Critical, in-hospital mortality, Blood, diagnose, acute respiratory distress, marker, Inflammatory biomarker, Invasive mechanical ventilation, Concentration, Pathways, epithelial cell, demographics, followed by, respiratory distress, tumor necrosis, amyloid A, end products, Non-COVID-19, endothelial, acute respiratory syndrome, Non-COVID-19 patients, cell injury, supplementary material, acute respiratory syndrome coronavirus, acute respiratory syndrome coronavirus 2, both groups, study enrollment, acute phase, diagnoses, serum amyloid, syndrome, positive, while, significantly lower, Host, sTNFR, plasma biomarker, SAA, Result, enrolled, resulting, collected, evaluate, involved, proportion, significantly higher, cause, groups, not different, biological pathway, in both group, non-COVID-19 patient, 【제목키워드】 epithelial, Inflammatory response, endothelial, Host, ICU patient, prospective observational cohort,