Abstract
To investigate the inflammatory factors and lymphocyte subsets which play an important role in the course of severe coronavirus disease 2019 (COVID‐19). A total of 27 patients with severe COVID‐19 who were admitted to Tongji Hospital in Wuhan from 1 to 21 February 2020 were recruited to the study. The characteristics of interleukin‐1β (IL‐1β), IL‐2 receptor (IL‐2R), IL‐6, IL‐8, IL‐10, tumor necrosis factor‐α (TNF)‐α, C‐reactive protein (CRP), serum ferritin and procalcitonin (PCT), and lymphocyte subsets of these patients were retrospectively compared before and after treatment. Before treatment, there was no significant difference in most inflammatory factors (IL‐1β, IL‐2R, IL‐6, IL‐8, IL‐10, CRP, and serum ferritin) between male and female patients. Levels of IL‐2R, IL‐6, TNF‐α, and CRP decreased significantly after treatment, followed by IL‐8, IL‐10, and PCT. Serum ferritin was increased in all patients before treatment but did not decrease significantly after treatment. IL‐1β was normal in most patients before treatment. Lymphopenia was common among these patients with severe COVID‐19. Analysis of lymphocyte subsets showed that CD4+ and particularly CD8+ T lymphocytes increased significantly after treatment. However, B lymphocytes and natural killer cells showed no significant changes after treatment. A pro‐inflammatory response and decreased level of T lymphocytes were associated with severe COVID‐19.
Highlights
COVID‐19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), and is the third highly pathogenic cor-Coronavirus disease 2019 (COVID‐19), which first appeared in Wuhan, China, in December 2019, has rapidly spread all over the world.[1,2] The World Health Organization characterized COVID‐19 as a pandemic on onavirus to arise, following the SARS‐CoV and the Middle East respiratory syndrome‐CoV
We found that levels of IL‐2 receptor (IL‐2R), IL‐6, tumor necrosis factor‐α (TNF)‐α, and C‐reactive protein (CRP) decreased significantly after corticosteroid therapy, followed by IL‐8, IL‐10, and PCT
Higher levels of proinflammatory cytokines have been associated with lung damage.[19]
Summary
COVID‐19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), and is the third highly pathogenic cor-. One of the main mechanisms for ARDS in SARS‐CoV and to China, the number of confirmed cases in other countries had reached MERS‐CoV infection is the cytokine storm: a deadly uncontrolled sys-. Regarding other inflammatory factors, elevated IL‐6, serum ferritin, and C‐reactive protein (CRP) have been most commonly reported in patients with COVID‐19.11. Lymphopenia is a common feature in patients with COVID‐19 and might be a critical factor associated with disease severity and mortality.[2,11,16]. With increasing evidence on the key pathophysiological role of inflammatory factors in patients with COVID‐19, immunomodulatory agents including corticosteroids, tocilizumab, and lucitanib have been considered for use in clinics. The characteristics of several inflammatory factors (IL‐ 1β, IL‐2 receptor (IL‐2R), IL‐6, IL‐8, IL‐10, TNF‐α, CRP, serum ferritin, and procalcitonin [PCT]) and lymphocyte subsets of 27 patients with severe COVID‐19 patients were examined. B lymphocytes and natural killer (NK) cells showed no significant change after treatment
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