Background Coronavirus disease 2019 (COVID-19) is a newly emerging infectious disease and rapidly escalating epidemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The pathogenesis of COVID-19 remains to be elucidated. We aimed to clarify correlation of systemic inflammation with disease severity and outcomes in COVID-19 patients. Methods In this retrospective study, baseline characteristics, laboratory findings, and treatments were compared among 317 laboratory-confirmed COVID-19 patients with moderate, severe, or critically ill form of the disease. Moreover, the longitudinal changes of serum cytokines, lactate dehydrogenase (LDH), high-sensitivity C-reactive protein (hsCRP), and hsCRP to lymphocyte count ratio (hsCRP/L) as well as their associations with disease severity and outcomes were investigated in 68 COVID-19 patients. Results Within 24 h of admission, the critically ill patients showed higher concentrations of inflammatory markers including serum soluble interleukin (IL)-2 receptor, IL-6, IL-8, IL-10, tumor necrosis factor alpha (TNF-α), ferritin, procalcitonin, LDH, hsCRP, and hsCRP/L than patients with severe or moderate disease. The severe cases displayed the similar response patterns when compared with moderate cases. The longitudinal assays showed the levels of pro-inflammatory cytokines, LDH, hsCRP, and hsCRP/L gradually declined within 10 days post admission in moderate, severe cases or those who survived. However, there was no significant reduction in cytokines, LDH, hsCRP, and hsCRP/L levels in critically ill or deceased patients throughout the course of illness. Compared with female patients, male cases showed higher serum concentrations of soluble IL-2R, IL-6, ferritin, procalcitonin, LDH, and hsCRP. Multivariate logistic regression analysis revealed that IL-6 > 50 pg/mL and LDH > 400 U/L on admission were independently associated with disease severity in patients with COVID-19. Conclusion Exuberant inflammatory responses within 24 h of admission in patients with COVID-19 may correlate with disease severity. SARS-CoV-2 infection appears to elicit a sex-based differential immune response. IL-6 and LDH were independent predictive parameters for assessing the severity of COVID-19. An early decline of these inflammation markers may be associated with better outcomes.

Background Dengue is one of the most common vector-borne diseases globally, however, its burden is poorly quantified. Hence, we aimed to report the dengue burden in 195 countries and territories between 1990 and 2017, using data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2017. Methods Following the methodology framework and analytical strategies used in the Global Burden of Disease Study 2017, we analysed the incidence, mortality, and disability-adjusted life years (DALYs) of dengue in geographically defined populations worldwide between 1990 and 2017. We also determined the association between development levels and dengue burden. All estimates were reported as numbers and rates per 100 000 population, with 95% uncertainty intervals. Findings Globally, the total number of dengue cases increased from 23 283 274 (95% UI 453 180.7–51 840 670) in 1990 to 104 771 911 (95% UI 63 759 019–158 870 031) in 2017. The age-standardised incidence rate increased from 431.6 (8.4–961.0) per 100 000 population in 1990 to 1371.3 (834.5–2079.3) per 100 000 population in 2017. In addition, the number of deaths due to dengue increased from approximately16 957 (7 613–30 091) in 1990 to 40 467 (17 620–49 778) in 2017. Meanwhile, the global age-standardised death rate increased from 0.31 (0.14–0•56) per 100 000 population in 1990 to 0.53 (0.23–0•65) per 100 000 population in 2017. Overall, there were 2 922 630 DALYs (1 629 424–3 967 492) attributed to dengue in 2017 globally, an increase of 107.6% since 1990 (1 407 571 DALYs [624 016.4–2 510 025]), and the age-standardised DALY rate increased from 26.10 (11.57–46.53) per 100 000 population to 38.25 (21.33–51.93) per 100 000 population between 1990 and 2017. The association between socio-demographic index (SDI) and dengue-related DALYs suggested that the lowest age-standardised DALY rates were found in countries in the low and high-SDI quintile in 2017, and from 1990 to 2017, the age-standardized DALY rate tended to increase in regions with the lowest SDI but declined in regions with the highest SDI. There was a nonlinear association between the socio-demographic index and the healthcare access and quality index and age-standardised DALY rates. Interpretation Dengue is a major public health challenge worldwide. While there is remarkable international variation in its incidence, the dengue burden is increasing globally. The results of this study could be useful for policy makers to implement cost-effective interventions and reduce the dengue burden, particularly in countries with high incidence or increasing burden. Funding This work was supported by a grant from the National Natural Science Foundation of China (NSFC) (grant numbers 81,800,041 and 82,000,078).

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by inflammatory cell activation and the release of inflammatory mediators. Interleukin-33 (IL-33) plays a critical role in various inflammatory and immunological pathologies, but evidence for its role in COPD is lacking. This study aimed to investigate the expression of IL-33 in COPD and to determine whether IL-33 participates in the initiation and progression of COPD. Levels of serum IL-33 and its receptors were measured by ELISA, and serum levels of IL-33, ST2, and IL-1 receptor accessory protein were elevated in patients with COPD compared with control subjects. Flow cytometry analysis further demonstrated an increase in peripheral blood lymphocytes (PBLs) expressing IL-33 in patients with COPD. Immunofluorescence analysis revealed that the main cellular source of IL-33 in lung tissue was human bronchial epithelial cells (HBEs). Cigarette smoke extract and lipopolysaccharide could enhance the ability of PBLs and HBEs to express IL-33. Furthermore, PBLs from patients with COPD showed greater IL-33 release in response to the stimulus. Collectively, these findings suggest that IL-33 expression levels are increased in COPD and related to airway and systemic inflammation. Therefore, IL-33 might contribute to the pathogenesis and progression of this disease.