Importance: An ongoing outbreak of COVID-19 has exhibited significant threats around the world. We found a significant decrease of T lymphocyte subsets and an increase of inflammatory cytokines of hospitalized patients with COVID-19 in clinical practice. Methods: We conducted a retrospective, single-center observational study of in-hospital adult patients with confirmed COVID-19 in Hubei Provincial Hospital of traditional Chinese and Western medicine (Wuhan, China) by Mar 1, 2020. Demographic, clinical, laboratory information, especially T lymphocyte subsets and inflammatory cytokines were reported. For patients who died or discharge from hospital, the associations of T lymphocyte subsets on admission were evaluated by univariate logistic regression with odds ratios (ORs) and 95% confidence intervals (CIs), warning values to predict in-hospital death were assessed by Receiver Operator Characteristic (ROC) curves. Results: A total of 187 patients were enrolled in our study from Dec 26, 2019 to Mar 1, 2020, of whom 145 were survivors (discharge = 117) or non-survivors (in-hospital death == 28). All patients exhibited a significant drop of T lymphocyte subsets counts with remarkably increasing concentrations of SAA, CRP, IL-6, and IL-10 compared to normal values. The median concentrations of SAA and CRP in critically-ill patients were nearly 4-and 10-fold than those of mild-ill patients, respectively. As the severity of COVID-19 getting worse, the counts of T lymphocyte drop lower.28 patients died in hospital, the median lymphocyte, CD3 + T -cell, CD4 + T -cell, CD8 + T -cell and B-cell were significantly lower than other patients. Lower counts (/uL) of T lymphocyte subsets lymphocyte ( < 500), CD3 + T -cell ( < 200), CD4 + T -cell ( < 100), CD8 + T -cell ( < 100) and B-cell ( < 50) were associated with higher risks of in-hospital death of CIVID-19. The warning values to predict in-hospital death of lymphocyte, CD3 + T -cell, CD4 + T -cell, CD8 + T -cell, and B-cell were 559, 235, 104, 85 and 82, respectively. Conclusion:We find a significant decrease of T lymphocyte subset is positively correlated with in-hospital death and severity of illness. The decreased levels of T lymphocyte subsets reported in our study were similar with SARS but not common among other virus infection, which may be possible biomarkers for early diagnosis of COVID-19. Our findings may shed light on early warning of high risks of mortality and help early intervention and treatment of COVID-19.

Cardiovascular disease, which can lead to angina and shortness of breath, remains one of the most serious threats to human health. Owing to its imperceptible symptoms, it is difficult to determine the pathogenesis and treatment methods for cardiovascular disease. Nuclear factor erythropoietin-2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) is a protein found in all cells of the human body. It is activated, transferred to the nucleus, and bound to DNA by antioxidant response elements (AREs). As a regulator of the antioxidant system, it upregulates the expression of HO-1 to reduce oxidative stress. Nrf2/HO-1 also has the ability to modulate calcium levels to prevent ferroptosis, pyroptosis, autophagy, programmed cell necrosis, alkaliptosis, and clockophagy. In view of the importance of Nrf2/HO-1 in the regulation of homeostasis, this review summarizes current research on the relationship between cardiovascular disease and Nrf2/HO-1. Normal cardiovascular diseases, such as viral myocarditis and myocardial ischemia-reperfusion injury, have been treated with Nrf2/HO-1. Rheumatic heart disease, cardiac tumors, arteriosclerosis, arrhythmia, hypertensive heart disease, and myocardial infarction have also been treated during experiments. Research has demonstrated the clinical application of Nrf2/HO-1 in pediatric cardiovascular disease; further clinical trials will help elucidate the potential of the Nrf2/HO-1 signaling axis.

IL-33, a new member of the IL-1 cytokine family, is associated with many infectious diseases. IL-33 not only is crucial for induction of Th2 polarized responses, but also is involved in induction of inflammation as a proinflammatory cytokine. Whether IL-33 leads to beneficial or worsening outcomes depends on the immune mechanism underlying the pathogensis of each disease condition. This study was to elucidate the role of IL-33 in schistosomiasis japonica in a mouse model. Our results demonstrated that serum levels of IL-33 from infected mice with Schistosoma japonicum began to rise at 1 week postinfection (pi) and reached a peak in 7 weeks pi, and then remained a plateau for 2 weeks, after which its level gradually decreased until 12 weeks pi. Compared with the infection control, exogenous IL-33 administration could increase a Th2 polarized immune response (evidenced by higher levels of IL-5, IL-10, and IL-13, along with lower level of IFN-γ) at 6 weeks pi. Meanwhile, this Th2 polarization was associated with higher infection intensity and liver immunopathology in infected mice, whereas injection of anti-IL-33 mAb into infected mice induced adverse effects on these above immune parameters and immunopathology. These data suggest that IL-33 might act as an inducer of Th2 polarization and plays a crucial role in immunopathology in murine schistosomiasis japonica.

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