In China, chronic obstructive pulmonary disease (COPD) was accounted for a quarter of the global COPD population and has become a large economic burden. However, the comprehensive picture of the COPD burden, which could inform health policy, is not readily available for all of the provinces of China. Here, we aimed to describe the burden of COPD in China, providing an up-to-date and comprehensive analysis at the national and provincial levels, and time trends from 1990 to 2019. Following the methodology framework and general analytical strategies used in the GBD 2019, we analyzed the incidence, prevalence, mortality, disability-adjusted life years (DALYs), years lived with disability (YLDs), and years with life lost (YLLs) attributable to COPD across China and the corresponding time trends from 1990 to 2019, stratified by age and province. In order to quantify the secular trends of the burden of COPD, the estimated annual percentage changes were calculated by the linear regression model of age-standardized rates (ASRs) and calendar years. We also presented the contribution of risk factors to COPD-related mortality and DALYs. The association between COPD burden and socio-demographic index (SDI) were also evaluated. From 1990 to 2019, the incidence and prevalence numbers of COPD increased by 61.2 and 67.8%, respectively, whereas the number of deaths and DALYs owing to COPD decreased. The ASRs of COPD burden, including incidence, prevalence, mortality, DALYs, YLDs, and YLLs continuously decreased from 1990 to 2019. The crude rates of COPD burden dramatically increased with age and reached a peak in the older than 95 years age group. In 2019, the leading risk factor for COPD mortality and DALYs was tobacco use in the whole population, but ambient particulate matter pollution was the most significant risk factor in females. At the provincial level, the ASRs of COPD burden was significantly associated with the SDIs, with the highest ASRs in the western provinces with low SDIs. Collectively, our study indicated that COPD remains an important public health problem in China. Geographically targeted considerations should be developed to enhance COPD health and reduce the COPD burden throughout China and in specific provinces.

Background: Perturbation of macrophage homeostasis is one of the key mechanisms of airway inflammation in asthma. However, the exact mechanisms remain poorly understood.

YKL-40 is also called chitinase-3-like-1 (CHI3L1) protein and may be a marker for asthma. The aims of the present study were to investigate whether serum YKL-40 levels are stable or decreased in patients with asthma after appropriate treatment and to evaluate the correlation of YKL-40 levels with lung function and asthma control test (ACT) results. A total of 103 asthmatic patients (mean age 33.1 ± 0.9 years) with diagnosed asthma were enrolled in our study. All patients underwent a detailed clinical examination and completed the ACT questionnaire, serum YKL-40 measurement, and spirometry before (visit 1) and 8 weeks after initiation of treatment (visit 2). At the follow-up, the median serum YKL-40 level was significantly decreased compared to the levels at visit 1 (75.2 [55.8-86.8] ng/ml versus 54.5 [46.4-58.4] ng/ml, p < 0.001). The serum YKL-40 level was negatively correlated with %FEV1 (r = -0.37, p < 0.001) and ACT score (r = -0.26, p = 0.007) at visit 1. The change in serum YKL-40 levels between the visits was significantly correlated with changes in FEV1 (r = -0.28, p = 0.006) and ACT score (r = -0.22, p = 0.037). Patients with elevated YKL-40 levels had significantly greater corticosteroid use than patients with lower levels. YKL-40 was reduced in the serum of asthmatic patients after appropriate treatment, and the levels correlated with improvements in %FEV1 and ACT. High levels of serum YKL-40 may be refractory to current asthma treatments. ChiCTR-OCC-13003316

N6-methyladenosine (m6A) modification accounts for the most prevalent mRNA internal modification and has emerged as a widespread regulatory mechanism in multiple physiological processes. We address a role of methyltransferase-like protein 3 (METTL3) in neutrophil activation. METTL3 controls neutrophil release from bone marrow to circulation through surface expression of CXC chemokine receptor 2 (CXCR2) in a Toll-like receptor 4 (TLR4) signaling-dependent manner in lipopolysaccharide (LPS)-induced endotoxemia. We show that the mRNA of TLR4 is modified by m6A, exhibiting increased translation and slowed degradation simultaneously, leading to elevated protein levels of TLR4, which eventually promotes the TLR4 signaling activation of neutrophil. The reduced expression of TLR4 lowers cytokine secretion in METTL3-deleted neutrophils upon LPS stimulation through TLR4/Myd88/nuclear factor κB (NF-κB) signaling. Collectively, these data demonstrate that METTL3 modulation of TLR4 expression is a critical determinant of neutrophil activation in endotoxemia.

Dysregulation of IL-17A is closely associated with airway inflammation and remodeling in severe asthma. However, the molecular mechanisms by which IL-17A is regulated remain unclear. Here we identify epithelial sirtuin 6 (SIRT6) as an epigenetic regulator that governs IL-17A pathogenicity in severe asthma. Mice with airway epithelial cell-specific deletion of Sirt6 are protected against allergen-induced airway inflammation and remodeling via inhibiting IL-17A-mediated inflammatory chemokines and mesenchymal reprogramming. Mechanistically, SIRT6 directly interacts with RORγt and mediates RORγt deacetylation at lysine 192 via its PPXY motifs. SIRT6 promotes RORγt recruitment to the IL-17A gene promoter and enhances its transcription. In severe asthma patients, high expression of SIRT6 positively correlates with airway remodeling and disease severity. SIRT6 inhibitor (OSS_128167) treatment significantly attenuates airway inflammation and remodeling in mice. Collectively, these results uncover a function for SIRT6 in regulating IL-17A pathogenicity in severe asthma, implicating SIRT6 as a potential therapeutic target for severe asthma.

Objective: As a result of the pandemic of COVID‐19, the public have been experiencing psychological distress. However, the prevalence of psychological distress during the COVID‐19 pandemic remains unknown. Our objective was to evaluate the prevalence of psychological distress during COVID‐19 outbreak and their risk factors, especially their internal paths and causality.Methods: A nationwide cross‐sectional survey of the prevalence of mental disorders was conducted. We used Hospital Anxiety and Depression Scale (HADS) to estimate the prevalence of anxiety and depression. The internal paths and the causality of the psychological health were analyzed using a structural equation modeling (SEM) approach.Results: A total of 24,789 respondents completed the survey. We found that the overall prevalence of anxiety, depression, combination of anxiety, and depression were 51.6% (95% CI: 51.0–52.2), 47.5% (95% CI: 46.9–48.1), and 24.5% (95% CI: 24.0–25.0), respectively. The risk of psychological disorders in men was higher than that in women. The status of psychological health was different across different age groups, education levels, occupations, and income levels. The SEM analysis revealed that inadequate material supplies, low income, low education, lack of knowledge or confidence of the epidemic, and lack of exercise are major risk factors for psychological distress.Conclusions: The evidence from this survey poses serious challenges related to the high prevalence of psychological distress, but also offers strategies to deal with the mental health problems caused by the COVID‐19 pandemic.