Gingival-derived mesenchymal stem cells alleviate allergic asthma inflammation via HGF in animal models.

Allergic asthma is a chronic non-communicable disease characterized by lung tissue inflammation. Current treatments can alleviate the clinical symptoms to some extent, but there is still no cure. Recently, the transplantation of mesenchymal stem cells (MSCs) has emerged as a potential approach for treating allergic asthma. Gingival-derived mesenchymal stem cells (GMSCs), a type of MSC recently studied, have shown significant therapeutic effects in various experimental models of autoimmune diseases. However, their application in allergic diseases has yet to be fully elucidated. In this study, using an OVA-induced allergic asthma model, we demonstrated that GMSCs decrease CD11b+CD11c+ proinflammatory dendritic cells (DCs), reduce Th2 cells differentiation, and thus effectively diminish eosinophils infiltration. We also identified that the core functional factor, hepatocyte growth factor (HGF) secreted by GMSCs, mediated its effects in relieving airway inflammation. Taken together, our findings indicate GMSCs as a potential therapy for allergic asthma and other related diseases.

Promising Intestinal Microbiota Associated with Clinical Characteristics of COPD Through Integrated Bioinformatics Analysis.

Introduction: Chronic obstructive pulmonary disease (COPD), an incurable chronic respiratory disease, has become a major public health problem. The relationship between the composition of intestinal microbiota and the important clinical factors affecting COPD remains unclear. This study aimed to identify specific intestinal microbiota with high clinical diagnostic value for COPD. Methods: The fecal microbiota of patients with COPD and healthy individuals were analyzed by 16S rDNA sequencing. Random forest classification was performed to analyze the different intestinal microbiota. Spearman correlation was conducted to analyze the correlation between different intestinal microbiota and clinical characteristics. A microbiota-disease network diagram was constructed using the gut MDisorder database to identify the possible pathogenesis of intestinal microorganisms affecting COPD, screen for potential treatment, and guide future research. Results: No significant difference in biodiversity was shown between the two groups but significant differences in microbial community structure. Fifteen genera of bacteria with large abundance differences were identified, including Bacteroides, Prevotella, Lachnospira, and Parabacteroides. Among them, the relative abundance of Lachnospira and Coprococcus was negatively related to the smoking index and positively related to lung function results. By contrast, the relative abundance of Parabacteroides was positively correlated with the smoking index and negatively correlated with lung function findings. Random forest classification showed that Lachnospira was the genus most capable of distinguishing between patients with COPD and healthy individuals suggesting it may be a potential biomarker of COPD. A Lachnospira disease network diagram suggested that Lachnospira decreased in some diseases, such as asthma, diabetes mellitus, and coronavirus disease 2019 (COVID-19), and increased in other diseases, such as irritable bowel syndrome, hypertension, and bovine lichen. Conclusion: The dominant intestinal microbiota with significant differences is related to the clinical characteristics of COPD, and the Lachnospira has the potential value to identify COPD.

Epithelial SIRT6 governs IL-17A pathogenicity and drives allergic airway inflammation and remodeling.

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.

The HDAC10 instructs macrophage M2 program via deacetylation of STAT3 and promotes allergic airway inflammation.

Background: Perturbation of macrophage homeostasis is one of the key mechanisms of airway inflammation in asthma. However, the exact mechanisms remain poorly understood. Objectives: We sought to examine the role of histone deacetylase (HDAC) 10 as an epigenetic regulator that governs macrophage M2 program and promotes airway inflammation in asthma, and to elucidate the underlying mechanisms. Methods: Peripheral blood and airway biopsies were obtained from healthy individuals and asthmatic patients. Asthma was induced by exposure to allergen in mice with myeloid-specific deletion of Hdac10 (Hdac10fl/fl-LysMCre) mice. HDAC10 inhibitor Salvianolic acid B (SAB), STAT3 selective agonist Colivelin, and the specific PI3K/Akt activator 1,3-Dicaffeoylquinic acid (DA) were also used in asthmatic mice. For cell studies, THP1 cells, primary mouse bone marrow derived macrophage (BMDMs) were used and related signaling pathways was investigated. Results: HDAC10 expression was highly expressed by macrophages and promoted M2 macrophage activation and airway inflammation in asthmatic patients and mice. Hdac10fl/fl-LysMCre mice were protected from airway inflammation in experimental asthma model. Hdac10 deficiency significantly attenuated STAT3 expression and decreased M2 macrophage polarization following allergen exposure. Mechanistically, HDAC10 directly binds STAT3 for deacetylation in macrophages, by which it promotes STAT3 expression and activates the macrophage M2 program. Importantly, we identified SAB as a HDAC10 inhibitor that had protective effects against airway inflammation in mice. Conclusions: Our results revealed that HDAC10-STAT3 interaction governs macrophage polarization to promote airway inflammation in asthma, implicating HDAC10 as a therapeutic target.

Myeloid-Specific SIRT6 Deletion Protects Against Particulate Matter (PM2.5)-Induced Airway Inflammation.

Purpose: Particulate matter (PM2.5) is a common risk factor for airway inflammation. Alveolar macrophages play a critical role in airway inflammation. Sirtuin 6 (SIRT6) is a class Ill histone deacetylase that exerts an anti-inflammatory effect in airway diseases. However, the role of SIRT6 on PM2.5-induced airway inflammation in macrophages remains unclear. We aimed to determine whether SIRT6 protects against PM2.5-induced airway inflammation in macrophages. Methods: The effect of SIRT6 on PM2.5-induced airway inflammation was assessed by using THP1 cells or bone marrow-derived macrophages (BMDMs) exposed to PM2.5 in vitro and myeloid cell-specific SIRT6 conditional knockout mice (Sirt6fl/fl-LysMCre) in vivo. Results: PM2.5 increased SIRT6 expression in THP1 cells, but SIRT6 gene silencing decreased PM2.5 induced inflammatory cytokines in THP1 cells. Moreover, the expression of SIRT6 and inflammatory cytokines was also decreased in BMDMs with myeloid-specific deletion of SIRT6 after stimulation of PM2.5. In vivo, Sirt6fl/fl-LysMCre mice substantially decreased airway inflammation in response to PM2.5 exposure. Conclusion: Our results revealed that SIRT6 promotes the PM2.5-induced airway inflammation in macrophages and indicated that inhibition of SIRT6 in macrophages may represent therapeutic strategy for airway disorders induced by airborne particulate pollution.

METTL3-mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling.

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.

Atmospheric particulate matter impairs cognition by modulating synaptic function via the nose-to-brain route.

Atmospheric particulate matter (PM), a ubiquitous air pollutant, is the leading environmental risk factor for mortality worldwide. Experimental and epidemiological studies consistently suggest a strong link between long-term exposure to PM2.5 (<2.5 µm, fine PM) and cognitive impairment. The neuroinflammatory response is presumed to be one of the main mechanisms of PM2.5-induced cognitive impairment, possibly leading to synaptic dysfunction. However, the main route and mechanism underlying the cause of cognitive dysfunction and pathogenic alterations in PM2.5-exposure mice remain poorly understood. Therefore, this study aimed to investigate the main route and mechanism of PM2.5-induced cognitive impairment. Our results showed that PM2.5 directly entered the brain following nasal administration, and both the short-term PM2.5 administration via atomization and nasal drops induced learning and memory impairments and neuronal damage in adult mice. Moreover, astrocytes and microglia were both activated in the two short-term PM2.5 exposure models, while few changes in the inflammatory response were observed in the peripheral circulatory system. Furthermore, a further transcriptional analysis revealed that short-term PM2.5 administration led to cognitive impairment mainly by modulating synaptic functions and that although glia were activated, the glia-related pathological pathways were not significantly activated. Notably, following PM2.5 exposure, PLX3397-induced microglial deletion did not restore the cognitive function of the mice. In conclusion, our results provide evidence that PM2.5 enters the brain via the nose-to-brain route to impair cognitive function, and short-term exposure to PM2.5 directly alters synaptic function rather than the neuroinflammatory response to affect cognition.

Trends in the prevalence of conduct disorder from 1990 to 2019: Findings from the Global Burden of Disease Study 2019.

Conduct disorder is one of the least widely recognized and studied psychiatric disorders. This study aimed to comprehensively analyze the burden of conduct disorder at the global, regional, and national levels based on the Global Burden of Disease (GBD) 2019 estimates. Globally, the age-standardized prevalence rates (ASPRs) of conduct disorder slightly increased from 1990 to 2019 with an estimated annual percentage change (EAPC) at 0.147. Males had a higher burden than females, but females had a greater increment in ASPRs than males over time. In 2019, the highest ASPR of conduct disorder was observed in Western Europe, followed by Eastern Europe, with the lowest one found in East Asia, then South Asia. However, the most significant increment in ASPRs was observed in high-income North America, followed by East Asia, and South Asia. The EAPCs at the national level were negatively associated with the ASPRs in 1990. The burden of conduct disorder continues to increase globally, especially in high-income North America, East Asia, and South Asia, and should have more attention focused on it.

The Burden of COPD in China and Its Provinces: Findings From the Global Burden of Disease Study 2019.

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.

Association between Vitamin D Status and Mortality among Adults with Diabetic Kidney Disease.

Objective: Emerging evidence demonstrates that vitamin D status contributes to the incidence of diabetic kidney disease (DKD). However, the causal relationships between vitamin D and mortality among individuals with DKD are inconclusive. Our study is aimed at exploring the relationship between serum 25-hydroxyvitamin D (25(OH)D) concentrations and mortality among adults with DKD. Research Design and Methods. Our study included 1,202 adult participants with DKD from the National Health and Nutrition Examination Survey (NHANES) 2001-2014. Cox and competing-risks regression were used to estimate hazard ratios (HRs) and 95% CIs for associations between 25(OH)D concentrations and survival. Results: The overall mean serum 25(OH)D concentration was 55.9 ± 26.3. Vitamin D deficiency (25(OH)D < 50 nmol/l), insufficiency group (50 ≤ 25(OH)D < 75 nmol/l), and sufficiency group (25(OH)D ≥ 75 nmol/l) were observed in 552 (45.9%), 409 (34.0%), and 241 (20.0%) participants, respectively. Higher levels of vitamin D were significantly associated with improved all-cause and nonaccident- and malignant neoplasm-cause mortality among individuals with DKD after adjusting for the potential confounding factors. Conclusions: We observed widespread vitamin D deficiency or insufficiency in DKD patients. Higher 25(OH)D values were significantly correlated with lower risk of mortality after adjusting for confounding variables.

The Combination of Bioinformatics Analysis and Untargeted Metabolomics Reveals Potential Biomarkers and Key Metabolic Pathways in Asthma.

Asthma is a complex chronic airway inflammatory disease that seriously impacts patients' quality of life. As a novel approach to exploring the pathogenesis of diseases, metabolomics provides the potential to identify biomarkers of asthma host susceptibility and elucidate biological pathways. The aim of this study was to screen potential biomarkers and biological pathways so as to provide possible pharmacological therapeutic targets for asthma. In the present study, we merged the differentially expressed genes (DEGs) of asthma in the GEO database with the metabolic genes obtained by Genecard for bioinformatics analysis and successfully screened out the metabolism-related hub genes (HIF1A, OCRL, NNMT, and PER1). Then, untargeted metabolic techniques were utilized to reveal HDM-induced metabolite alterations in 16HBE cells. A total of 45 significant differential metabolites and 5 differential metabolic pathways between the control group and HDM group were identified based on the OPLS-DA model. Finally, three key metabolic pathways, including glycerophospholipid metabolism, galactose metabolism, and alanine, aspartate, and glutamate metabolism, were screened through the integrated analysis of bioinformatics data and untargeted metabolomics data. Taken together, these findings provide valuable insights into the pathophysiology and targeted therapy of asthma and lay a foundation for further research.

HB-EGF-induced IL-8 secretion from airway epithelium leads to lung fibroblast proliferation and migration.

BACKGROUND: We have reported that heparin-binding epidermal growth factor (HB-EGF) is increased in patients with chronic obstructive pulmonary disease (COPD) and associated with collagen deposition, but the mechanisms remain unclear. In the present study, we aimed to investigated the inflammatory cytokines secreted by bronchial epithelial cells following exposure to HB-EGF that promoted proliferation and migration of human lung fibroblast. METHODS: HB-EGF-induced inflammatory cytokines were assayed in two airway epithelial cells (primary human bronchial epithelial cells [HBECs] and BEAS-2B cells). Moreover, the culture supernatants derived from HB-EGF-treated HBECs and BEAS-2B cells were added to human primary lung fibroblasts. The effect of culture supernatants on proliferation and migration of fibroblasts was assessed. RESULTS: IL-8 expression was significantly increased in bronchial epithelial cells treated with HB-EGF, which was at least partially dependent on NF-kB pathways activation. HB-EGF-induced IL-8 was found to further promote lung fibroblasts proliferation and migration, and the effects were attenuated after neutralizing IL-8. CONCLUSIONS: These findings suggest that HB-EGF may be involved in the pathology of airway fibrosis by induction of IL-8 from airway epithelium, subsequently causing lung fibroblasts proliferation and migration. Thus, inhibition of HBEGF and/or IL-8 production could prevent the development of airway fibrosis by modulating fibroblast activation.

Probiotics use is associated with improved clinical outcomes among hospitalized patients with COVID-19.

BACKGROUND AND AIMS: Currently, there are no definitive therapies for coronavirus disease 2019 (COVID-19). Gut microbial dysbiosis has been proved to be associated with COVID-19 severity and probiotics is an adjunctive therapy for COIVD-19. However, the potential benefit of probiotics in COVID-19 has not been studied. We aimed to assess the relationship of probiotics use with clinical outcomes in patients with COVID-19. METHODS: We conducted a propensity-score matched retrospective cohort study of adult patients with COVID-19. Eligible patients received either probiotics plus standard care (probiotics group) or standard care alone (non-probiotics group). The primary outcome was the clinical improvement rate, which was compared among propensity-score matched groups and in the unmatched cohort. Secondary outcomes included the duration of viral shedding, fever, and hospital stay. RESULTS: Among the propensity-score matched groups, probiotics use was related to clinical improvement rates (log-rank p = 0.028). This relationship was driven primarily by a shorter (days) time to clinical improvement [difference, -3 (-4 to -1), p = 0.022], reduction in duration of fever [-1.0 (-2.0 to 0.0), p = 0.025], viral shedding [-3 (-6 to -1), p < 0.001], and hospital stay [-3 (-5 to -1), p = 0.009]. Using the Cox model with time-varying exposure, use of probiotics remained independently related to better clinical improvement rate in the unmatched cohort. CONCLUSION: Our study suggested that probiotics use was related to improved clinical outcomes in patients with COVID-19. Further studies are required to validate the effect of probiotics in combating the COVID-19 pandemic.

Myeloid-specific SIRT1 deletion exacerbates airway inflammatory response in a mouse model of allergic asthma.

Sirtuin 1 (SIRT1) is a class III histone deacetylase that exerts an anti-inflammatory effect in airway diseases. Activated macrophages play an important role in asthma. However, the roles of SIRT1 on allergic airway inflammation in macrophages remain largely unexplored. In this study, we aimed to determine the roles of SIRT1 on allergic airway inflammation in macrophages. The effect of myeloid-specific SIRT1 deletion (Sirt1fl/fl-LysMcre) on airway inflammation was assessed by using in vivo models of asthma following allergen exposure and in vitro culture of primary bone marrow-derived macrophages (BMDMs) exposed to house dust mite (HDM). We observed that Sirt1fl/fl-LysMcre mice substantially enhanced airway inflammation and mucus production in response to allergen exposure. Expression of chemokine ligand (CXCL) 2, interleukin (IL)-1ß, and tumor necrosis factor (TNF)-α were reduced in BMDMs with myeloid-specific deletion of Sirt1 after stimulation of HDM. Moreover, SIRT1 suppressed the inflammatory cytokines expression in BMDMs partially via the ERK/p38 MAPK pathways. Our study demonstrated that SIRT1 suppresses the allergic airway inflammation in macrophages, and suggested that activation of SIRT1 in macrophages may represent therapeutic strategy for asthma.

IL-17-Mediated Inflammation Promotes Cigarette Smoke-Induced Genomic Instability.

(1) Background: Chronic inflammation has been regarded as a risk factor for the onset and progression of human cancer, but the critical molecular mechanisms underlying this pathological process have yet to be elucidated. (2) Methods: In this study, we investigated whether interleukin (IL)-17-mediated inflammation was involved in cigarette smoke-induced genomic instability. (3) Results: Higher levels of both IL-17 and the DNA damage response (DDR) were found in the lung tissues of smokers than in those of non-smokers. Similarly, elevated levels of IL-17 and the DDR were observed in mice after cigarette smoke exposure, and a positive correlation was observed between IL-17 expression and the DDR. In line with these observations, the DDR in the mouse lung was diminished in IL-17 KO when exposed to cigarette smoke. Besides this, the treatment of human bronchial epithelium cells with IL-17 led to increased levels of the DDR and chromosome breakage. (4) Conclusions: These results suggest that cigarette smoke induces genomic instability at least partially through IL-17-mediated inflammation, implying that IL-17 could play an important role in the development of lung cancer.

Epithelium-derived IL17A Promotes Cigarette Smoke-induced Inflammation and Mucus Hyperproduction.

The airway epithelium is a central modulator of innate and adaptive immunity in the lung. IL17A expression was found to be increased in the airway epithelium; however, the role of epithelium-derived IL17A in chronic obstructive pulmonary disease (COPD) remains unclear. In this study, we aimed to determine whether epithelium-derived IL17A regulates inflammation and mucus hyperproduction in COPD by using a cultured human bronchial epithelial (HBE) cell line in vitro and an airway epithelium IL17A-specific knockout mouse in vivo. Increased IL17A expression was observed in the mouse airway epithelium upon cigarette smoke (CS) exposure or in a mouse model of COPD that was induced by using CS and Eln (elastin). CS extract (CSE) also triggered IL17A expression in HBE cells. Blocking IL17A or IL17RA (IL17 receptor A) effectively attenuated CSE-induced MUC5AC and the inflammatory cytokines IL6, TNF-α, and IL1ß in HBE cells, suggesting that IL17A mediates CSE-induced inflammation and mucin production in an autocrine manner. CSE activated p-JUN (phospho-JUN) and p-JNK (phospho-c-Jun N-terminal kinase), which were also reduced by IL17RA siRNA, and JUN siRNA attenuated CSE-induced IL6 and MUC5AC. In vivo, selective knockout of IL17A in the airway epithelium markedly reduced the neutrophilic infiltration in BAL fluid, peribronchial inflammation, proinflammatory mediators (CXCL1 [CXC ligand 1] and CXCL2), and mucus production in a COPD mouse model. We showed a novel function of airway epithelium-derived IL17A, which can act locally in an autocrine manner to amplify inflammation and increase mucus production in COPD pathogenesis.

Global, regional and national disability-adjusted life years due to HIV from 1990 to 2019: findings from the Global Burden of Disease Study 2019.

OBJECTIVES: Increasing life expectancy and decreasing mortality in patients with HIV infection are well documented. However, details of how many of the years of healthy life are damaged by HIV infection vs. good health have not been understood. We conducted this study to provide a comprehensive assessment of the levels and trends of the global burden, as measured by disability-adjusted life years (DALYs), of HIV infection. METHODS: Data on HIV-related DALY were obtained from the Global Burden of Disease Study 2019. The absolute numbers and age-standardised rates of DALYs due to HIV were reported between 1990 and 2019. Estimated annual percentage changes in age-standardised rates by sex, region and nation were calculated to quantify the temporal trends in HIV burden. RESULTS: Global HIV infection caused 47.63 million DALYs in 2019, presenting a 1.28-fold increase from 1990 to 2019. In 2019, years of life lost contributed to most of the total DALYs, but the increases in HIV-related years lived with disability have outpaced increases in years of life lost. The age-standardised rates of HIV-related DALYs in 2019 decreased as the sociodemographic indexes increased. The highest age-standardised rates were observed in sub-Saharan Africa, and the greatest increments over time were detected in Oceania. CONCLUSIONS: Globally, HIV continues to cause enormous healthy life loss. The first and foremost strategy for controlling the HIV burden is still the reduction of premature deaths, and much effort needs to be exerted to mitigate the harm of comorbidities.

Reliability of induced sputum test is greater than that of throat swab test for detecting SARS-CoV-2 in patients with COVID-19: A multi-center cross-sectional study.

We previously reported that sputum induction was more sensitive than throat swabs for the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in two convalescent coronavirus disease 2019 (COVID-19) patients; however, the value and safety of induced sputum testing require further study. We conducted a prospective multi-center cross-sectional study to compare induced sputum to throat swabs for SARS-CoV-2 detection. Confirmed COVID-19 patients from six hospitals in six cities across China who received one or more negative RT-PCR result for SARS-CoV-2 were enrolled, and paired specimens (induced sputum and throat swabs; 56 cases) were assayed. In three paired samples, both the induced sputum and throat swabs were positive for SARS-CoV-2. The positive rate for induced sputum was significantly higher than for throat swabs both overall (28.6% vs 5.4%, respectively; p < 0.01). Patients were divided according to time span from onset of illness to sample collection into the more-than-30-day (n = 26) and less-than-30-day (n = 30) groups. The positive rate for induced sputum was also significantly higher than for throat swabs in the less-than-30-day group (53.3% vs 10.0%, respectively; p < 0.001). For the more-than-30-day group, all paired samples were negative for SARS-CoV-2. Blood oxygen saturation, respiratory rate, and heart rate remained stable during sputum induction and no staff were infected. Because induced sputum is more reliable and has a lower false-negative rate than throat swabs, we believe induced sputum is more useful for the confirmation of COVID-19 and is safer as a criterion for release from quarantine.