Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fatal, and aging-associated interstitial lung disease with a poor prognosis and limited treatment options, while the pathogenesis remains elusive. In this study, we found that the expression of nuclear receptor subfamily 2 group F member 2 (NR2F2), a member of the steroid thyroid hormone superfamily of nuclear receptors, was reduced in both IPF and bleomycin-induced fibrotic lungs, markedly in bleomycin-induced senescent epithelial cells. Inhibition of NR2F2 expression increased the expression of senescence markers such as p21 and p16 in lung epithelial cells, and activated fibroblasts through epithelial-mesenchymal crosstalk, inversely overexpression of NR2F2 alleviated bleomycin-induced epithelial cell senescence and inhibited fibroblast activation. Subsequent mechanistic studies revealed that overexpression of NR2F2 alleviated DNA damage in lung epithelial cells and inhibited cell senescence. Adenovirus-mediated Nr2f2 overexpression attenuated bleomycin-induced lung fibrosis and cell senescence in mice. In summary, these data demonstrate that NR2F2 is involved in lung epithelial cell senescence, and targeting NR2F2 may be a promising therapeutic approach against lung cell senescence and fibrosis.
特发性肺纤维化（IPF）是一种与衰老相关的慢性、进行性、致命性间质性肺病，预后不良，治疗方案有限，其发病机制仍难以捉摸。在这项研究中，我们发现在 IPF 和博莱霉素诱导的纤维化肺中，核受体亚家族 2 F 组成员 2（NR2F2）的表达都有所降低，NR2F2 是类固醇甲状腺激素超家族核受体的成员之一，在博莱霉素诱导的衰老上皮细胞中表达明显降低。抑制NR2F2的表达会增加肺上皮细胞中p21和p16等衰老标志物的表达，并通过上皮-间质串联激活成纤维细胞；相反，过表达NR2F2会缓解博莱霉素诱导的上皮细胞衰老，并抑制成纤维细胞的激活。随后的机理研究发现，过表达 NR2F2 可减轻肺上皮细胞的 DNA 损伤并抑制细胞衰老。腺病毒介导的 Nr2f2 过表达减轻了博莱霉素诱导的小鼠肺纤维化和细胞衰老。总之，这些数据证明了NR2F2参与了肺上皮细胞的衰老，靶向NR2F2可能是一种很有前景的针对肺细胞衰老和纤维化的治疗方法。
{"title":"NR2F2 alleviates pulmonary fibrosis by inhibition of epithelial cell senescence","authors":"Ruyan Wan, Siqi Long, Shuaichen Ma, Peishuo Yan, Zhongzheng Li, Kai Xu, Hui Lian, Wenwen Li, Yudi Duan, Miaomiao Zhu, Lan Wang, Guoying Yu","doi":"10.1186/s12931-024-02777-3","DOIUrl":"https://doi.org/10.1186/s12931-024-02777-3","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fatal, and aging-associated interstitial lung disease with a poor prognosis and limited treatment options, while the pathogenesis remains elusive. In this study, we found that the expression of nuclear receptor subfamily 2 group F member 2 (NR2F2), a member of the steroid thyroid hormone superfamily of nuclear receptors, was reduced in both IPF and bleomycin-induced fibrotic lungs, markedly in bleomycin-induced senescent epithelial cells. Inhibition of NR2F2 expression increased the expression of senescence markers such as p21 and p16 in lung epithelial cells, and activated fibroblasts through epithelial-mesenchymal crosstalk, inversely overexpression of NR2F2 alleviated bleomycin-induced epithelial cell senescence and inhibited fibroblast activation. Subsequent mechanistic studies revealed that overexpression of NR2F2 alleviated DNA damage in lung epithelial cells and inhibited cell senescence. Adenovirus-mediated Nr2f2 overexpression attenuated bleomycin-induced lung fibrosis and cell senescence in mice. In summary, these data demonstrate that NR2F2 is involved in lung epithelial cell senescence, and targeting NR2F2 may be a promising therapeutic approach against lung cell senescence and fibrosis.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"62 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140589339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-11DOI: 10.1186/s12931-024-02742-0
Elizabeth S. McCluskey, Nathan Liu, Abhimaneu Pandey, Nathaniel Marchetti, Steven G. Kelsen, Umadevi S. Sajjan
Airway basal cells (BC) from patients with chronic obstructive pulmonary disease (COPD) regenerate abnormal airway epithelium and this was associated with reduced expression of several genes involved in epithelial repair. Quercetin reduces airway epithelial remodeling and inflammation in COPD models, therefore we examined whether quercetin promotes normal epithelial regeneration from COPD BC by altering gene expression. COPD BC treated with DMSO or 1 µM quercetin for three days were cultured at air/liquid interface (ALI) for up to 4 weeks. BC from healthy donors cultured at ALI were used as controls. Polarization of cells was determined at 8 days of ALI. The cell types and IL-8 expression in differentiated cell cultures were quantified by flow cytometry and ELISA respectively. Microarray analysis was conducted on DMSO or 1 µM quercetin-treated COPD BC for 3 days to identify differentially regulated genes (DEG). Bronchial brushings obtained from COPD patients with similar age and disease status treated with either placebo (4 subjects) or 2000 mg/day quercetin (7 subjects) for 6 months were used to confirm the effects of quercetin on gene expression. Compared to placebo-, quercetin-treated COPD BC showed significantly increased transepithelial resistance, more ciliated cells, fewer goblet cells, and lower IL-8. Quercetin upregulated genes associated with tissue and epithelial development and differentiation in COPD BC. COPD patients treated with quercetin, but not placebo showed increased expression of two developmental genes HOXB2 and ELF3, which were also increased in quercetin-treated COPD BC with FDR < 0.001. Active smokers showed increased mRNA expression of TGF-β (0.067) and IL-8 (22.0), which was reduced by 3.6 and 4.14 fold respectively after quercetin treatment. These results indicate that quercetin may improve airway epithelial regeneration by increasing the expression of genes involved in epithelial development/differentiation in COPD. This study was registered at ClinicalTrials.gov on 6-18-2019. The study number is NCT03989271.
慢性阻塞性肺病（COPD）患者的气道基底细胞（BC）会再生出异常的气道上皮，这与参与上皮修复的多个基因表达量减少有关。槲皮素能减少慢性阻塞性肺病模型中的气道上皮重塑和炎症，因此我们研究了槲皮素是否能通过改变基因表达促进慢性阻塞性肺病BC的正常上皮再生。用 DMSO 或 1 µM 槲皮素处理 COPD BC 三天后，在空气/液体界面（ALI）培养长达 4 周。在 ALI 条件下培养的健康供体 BC 作为对照。在 ALI 8 天时测定细胞的极化。分化细胞培养物中的细胞类型和 IL-8 表达分别通过流式细胞仪和 ELISA 进行量化。对经 DMSO 或 1 µM 槲皮素处理 3 天的 COPD BC 进行微阵列分析，以确定差异调控基因（DEG）。为了证实槲皮素对基因表达的影响，研究人员对年龄和疾病状况相似的慢性阻塞性肺病患者进行了为期 6 个月的支气管刷检，这些患者分别接受了安慰剂（4 人）或每天 2000 毫克槲皮素（7 人）的治疗。与安慰剂相比，接受槲皮素治疗的慢性阻塞性肺疾病 BC 患者的跨上皮阻力明显增加，纤毛细胞增多，鹅口疮细胞减少，IL-8 降低。槲皮素能上调 COPD BC 中与组织和上皮发育及分化相关的基因。接受槲皮素治疗的慢性阻塞性肺病患者（而非安慰剂）的两个发育基因HOXB2和ELF3的表达量有所增加，槲皮素治疗的慢性阻塞性肺病BC中这两个基因的表达量也有所增加，FDR<0.001。活跃吸烟者的TGF-β（0.067）和IL-8（22.0）的mRNA表达增加，槲皮素治疗后这两种基因的表达分别减少了3.6倍和4.14倍。这些结果表明，槲皮素可通过增加慢性阻塞性肺病患者上皮发育/分化相关基因的表达来改善气道上皮再生。本研究于2019年6月18日在ClinicalTrials.gov注册。研究编号为 NCT03989271。
{"title":"Quercetin improves epithelial regeneration from airway basal cells of COPD patients","authors":"Elizabeth S. McCluskey, Nathan Liu, Abhimaneu Pandey, Nathaniel Marchetti, Steven G. Kelsen, Umadevi S. Sajjan","doi":"10.1186/s12931-024-02742-0","DOIUrl":"https://doi.org/10.1186/s12931-024-02742-0","url":null,"abstract":"Airway basal cells (BC) from patients with chronic obstructive pulmonary disease (COPD) regenerate abnormal airway epithelium and this was associated with reduced expression of several genes involved in epithelial repair. Quercetin reduces airway epithelial remodeling and inflammation in COPD models, therefore we examined whether quercetin promotes normal epithelial regeneration from COPD BC by altering gene expression. COPD BC treated with DMSO or 1 µM quercetin for three days were cultured at air/liquid interface (ALI) for up to 4 weeks. BC from healthy donors cultured at ALI were used as controls. Polarization of cells was determined at 8 days of ALI. The cell types and IL-8 expression in differentiated cell cultures were quantified by flow cytometry and ELISA respectively. Microarray analysis was conducted on DMSO or 1 µM quercetin-treated COPD BC for 3 days to identify differentially regulated genes (DEG). Bronchial brushings obtained from COPD patients with similar age and disease status treated with either placebo (4 subjects) or 2000 mg/day quercetin (7 subjects) for 6 months were used to confirm the effects of quercetin on gene expression. Compared to placebo-, quercetin-treated COPD BC showed significantly increased transepithelial resistance, more ciliated cells, fewer goblet cells, and lower IL-8. Quercetin upregulated genes associated with tissue and epithelial development and differentiation in COPD BC. COPD patients treated with quercetin, but not placebo showed increased expression of two developmental genes HOXB2 and ELF3, which were also increased in quercetin-treated COPD BC with FDR < 0.001. Active smokers showed increased mRNA expression of TGF-β (0.067) and IL-8 (22.0), which was reduced by 3.6 and 4.14 fold respectively after quercetin treatment. These results indicate that quercetin may improve airway epithelial regeneration by increasing the expression of genes involved in epithelial development/differentiation in COPD. This study was registered at ClinicalTrials.gov on 6-18-2019. The study number is NCT03989271.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"87 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140097835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-11DOI: 10.1186/s12931-023-02632-x
Robert C. Wharton, Jing Gennie Wang, Yuni Choi, Elliot Eisenberg, Mariah K. Jackson, Corrine Hanson, Bian Liu, George R. Washko, Ravi Kalhan, David R. Jacobs, Sonali Bose
Lung function throughout adulthood predicts morbidity and mortality even among adults without chronic respiratory disease. Diet quality may represent a modifiable risk factor for lung function impairment later in life. We investigated associations between nutritionally-rich plant-centered diet and lung function across early and middle adulthood from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Diet was assessed at baseline and years 7 and 20 of follow-up using the validated CARDIA diet history questionnaire. Plant-centered diet quality was scored using the validated A Priori Diet Quality Score (APDQS), which weights food groups to measure adherence to a nutritionally-rich plant-centered diet for 20 beneficially rated foods and 13 adversely rated foods. Scores were cumulatively averaged over follow-up and categorized into quintiles. The primary outcome was lung function decline, including forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), measured at years 0, 2, 5, 10, 20, and 30. We estimated the association of APDQS with annual pulmonary function changes and cross-sectional differences in a repeated measures regression model, adjusting for clinically relevant covariates. The study included 3,787 Black and White men and women aged 18–30 in 1985–86 and followed for 30 years. In multivariable repeated measures regression models, individuals in the lowest APDQS quintile (poorest diet) had declines in FEV1 that were 1.6 ml/year greater than individuals in the highest quintile (35.0 vs. 33.4 ml/year, ß ± SE per 1 SD change APDQS 0.94 ± 0.36, p = 0.009). Additionally, declines in FVC were 2.4 ml/year greater in the lowest APDQS quintile than those in the highest quintile (37.0 vs 34.6 ml/year, ß ± SE per 1 SD change APDQS 1.71 ± 0.46, p < 0.001). The association was not different between never and ever smokers (pint = 0.07 for FVC and 0.32 for FEV1). In sensitivity analyses where current asthma diagnosis and cardiorespiratory fitness were further adjusted, results remained similar. Cross-sectional analysis at each exam year also showed significant differences in lung function according to diet after covariate adjustment. In this 30-year longitudinal cohort study, long-term adherence to a nutritionally-rich plant-centered diet was associated with cross-sectional differences in lung function as well as slower decline in lung function, highlighting diet quality as a potential treatable trait supporting long-term lung health.
{"title":"Associations of a plant-centered diet and lung function across early to mid-adulthood: The CARDIA Lung Study","authors":"Robert C. Wharton, Jing Gennie Wang, Yuni Choi, Elliot Eisenberg, Mariah K. Jackson, Corrine Hanson, Bian Liu, George R. Washko, Ravi Kalhan, David R. Jacobs, Sonali Bose","doi":"10.1186/s12931-023-02632-x","DOIUrl":"https://doi.org/10.1186/s12931-023-02632-x","url":null,"abstract":"Lung function throughout adulthood predicts morbidity and mortality even among adults without chronic respiratory disease. Diet quality may represent a modifiable risk factor for lung function impairment later in life. We investigated associations between nutritionally-rich plant-centered diet and lung function across early and middle adulthood from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Diet was assessed at baseline and years 7 and 20 of follow-up using the validated CARDIA diet history questionnaire. Plant-centered diet quality was scored using the validated A Priori Diet Quality Score (APDQS), which weights food groups to measure adherence to a nutritionally-rich plant-centered diet for 20 beneficially rated foods and 13 adversely rated foods. Scores were cumulatively averaged over follow-up and categorized into quintiles. The primary outcome was lung function decline, including forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), measured at years 0, 2, 5, 10, 20, and 30. We estimated the association of APDQS with annual pulmonary function changes and cross-sectional differences in a repeated measures regression model, adjusting for clinically relevant covariates. The study included 3,787 Black and White men and women aged 18–30 in 1985–86 and followed for 30 years. In multivariable repeated measures regression models, individuals in the lowest APDQS quintile (poorest diet) had declines in FEV1 that were 1.6 ml/year greater than individuals in the highest quintile (35.0 vs. 33.4 ml/year, ß ± SE per 1 SD change APDQS 0.94 ± 0.36, p = 0.009). Additionally, declines in FVC were 2.4 ml/year greater in the lowest APDQS quintile than those in the highest quintile (37.0 vs 34.6 ml/year, ß ± SE per 1 SD change APDQS 1.71 ± 0.46, p < 0.001). The association was not different between never and ever smokers (pint = 0.07 for FVC and 0.32 for FEV1). In sensitivity analyses where current asthma diagnosis and cardiorespiratory fitness were further adjusted, results remained similar. Cross-sectional analysis at each exam year also showed significant differences in lung function according to diet after covariate adjustment. In this 30-year longitudinal cohort study, long-term adherence to a nutritionally-rich plant-centered diet was associated with cross-sectional differences in lung function as well as slower decline in lung function, highlighting diet quality as a potential treatable trait supporting long-term lung health.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"87 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140098096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-11DOI: 10.1186/s12931-024-02746-w
Mona Alotaibi, Jenny Z. Yang, Demosthenes G. Papamatheakis, W. Cameron McGuire, Timothy M. Fernandes, Timothy A. Morris
Cardiac dysfunction from pulmonary vascular disease causes characteristic findings on cardiopulmonary exercise testing (CPET). We tested the accuracy of CPET for detecting inadequate stroke volume (SV) augmentation during exercise, a pivotal manifestation of cardiac limitation in patients with pulmonary vascular disease. We reviewed patients with suspected pulmonary vascular disease in whom CPET and right heart catheterization (RHC) measurements were taken at rest and at anaerobic threshold (AT). We correlated CPET-determined O2·pulseAT/O2·pulserest with RHC-determined SVAT/SVrest. We evaluated the sensitivity and specificity of O2·pulseAT/O2·pulserest to detect SVAT/SVrest below the lower limit of normal (LLN). For comparison, we performed similar analyses comparing echocardiographically-measured peak tricuspid regurgitant velocity (TRVpeak) with SVAT/SVrest. From July 2018 through February 2023, 83 simultaneous RHC and CPET were performed. Thirty-six studies measured O2·pulse and SV at rest and at AT. O2·pulseAT/O2·pulserest correlated highly with SVAT/SVrest (r = 0.72, 95% CI 0.52, 0.85; p < 0.0001), whereas TRVpeak did not (r = -0.09, 95% CI -0.47, 0.33; p = 0.69). The AUROC to detect SVAT/SVrest below the LLN was significantly higher for O2·pulseAT/O2·pulserest (0.92, SE 0.04; p = 0.0002) than for TRVpeak (0.69, SE 0.10; p = 0.12). O2·pulseAT/O2·pulserest of less than 2.6 was 92.6% sensitive (95% CI 76.6%, 98.7%) and 66.7% specific (95% CI 35.2%, 87.9%) for deficient SVAT/SVrest. CPET detected deficient SV augmentation more accurately than echocardiography. CPET-determined O2·pulseAT/O2·pulserest may have a prominent role for noninvasive screening of patients at risk for pulmonary vascular disease, such as patients with persistent dyspnea after pulmonary embolism.
{"title":"Cardiopulmonary exercise test to detect cardiac dysfunction from pulmonary vascular disease","authors":"Mona Alotaibi, Jenny Z. Yang, Demosthenes G. Papamatheakis, W. Cameron McGuire, Timothy M. Fernandes, Timothy A. Morris","doi":"10.1186/s12931-024-02746-w","DOIUrl":"https://doi.org/10.1186/s12931-024-02746-w","url":null,"abstract":"Cardiac dysfunction from pulmonary vascular disease causes characteristic findings on cardiopulmonary exercise testing (CPET). We tested the accuracy of CPET for detecting inadequate stroke volume (SV) augmentation during exercise, a pivotal manifestation of cardiac limitation in patients with pulmonary vascular disease. We reviewed patients with suspected pulmonary vascular disease in whom CPET and right heart catheterization (RHC) measurements were taken at rest and at anaerobic threshold (AT). We correlated CPET-determined O2·pulseAT/O2·pulserest with RHC-determined SVAT/SVrest. We evaluated the sensitivity and specificity of O2·pulseAT/O2·pulserest to detect SVAT/SVrest below the lower limit of normal (LLN). For comparison, we performed similar analyses comparing echocardiographically-measured peak tricuspid regurgitant velocity (TRVpeak) with SVAT/SVrest. From July 2018 through February 2023, 83 simultaneous RHC and CPET were performed. Thirty-six studies measured O2·pulse and SV at rest and at AT. O2·pulseAT/O2·pulserest correlated highly with SVAT/SVrest (r = 0.72, 95% CI 0.52, 0.85; p < 0.0001), whereas TRVpeak did not (r = -0.09, 95% CI -0.47, 0.33; p = 0.69). The AUROC to detect SVAT/SVrest below the LLN was significantly higher for O2·pulseAT/O2·pulserest (0.92, SE 0.04; p = 0.0002) than for TRVpeak (0.69, SE 0.10; p = 0.12). O2·pulseAT/O2·pulserest of less than 2.6 was 92.6% sensitive (95% CI 76.6%, 98.7%) and 66.7% specific (95% CI 35.2%, 87.9%) for deficient SVAT/SVrest. CPET detected deficient SV augmentation more accurately than echocardiography. CPET-determined O2·pulseAT/O2·pulserest may have a prominent role for noninvasive screening of patients at risk for pulmonary vascular disease, such as patients with persistent dyspnea after pulmonary embolism.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"389 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140098083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-07DOI: 10.1186/s12931-024-02747-9
Judith van Paassen, Pieter S. Hiemstra, Abraham C. van der Linden, Evert de Jonge, Jaap Jan Zwaginga, Robert J.M. Klautz, M. Sesmu Arbous
Heart surgery may be complicated by acute lung injury and adult respiratory distress syndrome. Expression and release of mucins MUC5AC and MUC5B in the lungs has been reported to be increased in acute lung injury. The aim of our study was to [1] investigate the perioperative changes of MUC5AC, MUC5B and other biomarkers in mini-bronchoalveolar lavage (minBAL), and [2] relate these to clinical outcomes after cardiac surgery. In this prospective cohort study in 49 adult cardiac surgery patients pre- and post-surgery non-fiberscopic miniBAL fluids were analysed for MUC5AC, MUC5B, IL-8, human neutrophil elastase, and neutrophils. All measured biomarkers increased after surgery. Perioperative MUC5AC-change showed a significant negative association with postoperative P/F ratio (p = 0.018), and a positive association with ICU stay (p = 0.027). In conclusion, development of lung injury after cardiac surgery and prolonged ICU stay are associated with an early increase of MUC5AC as detected in mini-BAL.
{"title":"MUC5AC concentrations in lung lavage fluids are associated with acute lung injury after cardiac surgery","authors":"Judith van Paassen, Pieter S. Hiemstra, Abraham C. van der Linden, Evert de Jonge, Jaap Jan Zwaginga, Robert J.M. Klautz, M. Sesmu Arbous","doi":"10.1186/s12931-024-02747-9","DOIUrl":"https://doi.org/10.1186/s12931-024-02747-9","url":null,"abstract":"Heart surgery may be complicated by acute lung injury and adult respiratory distress syndrome. Expression and release of mucins MUC5AC and MUC5B in the lungs has been reported to be increased in acute lung injury. The aim of our study was to [1] investigate the perioperative changes of MUC5AC, MUC5B and other biomarkers in mini-bronchoalveolar lavage (minBAL), and [2] relate these to clinical outcomes after cardiac surgery. In this prospective cohort study in 49 adult cardiac surgery patients pre- and post-surgery non-fiberscopic miniBAL fluids were analysed for MUC5AC, MUC5B, IL-8, human neutrophil elastase, and neutrophils. All measured biomarkers increased after surgery. Perioperative MUC5AC-change showed a significant negative association with postoperative P/F ratio (p = 0.018), and a positive association with ICU stay (p = 0.027). In conclusion, development of lung injury after cardiac surgery and prolonged ICU stay are associated with an early increase of MUC5AC as detected in mini-BAL.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"10 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140054309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-06DOI: 10.1186/s12931-024-02751-z
Francesco Amati, Anna Stainer, Stefano Aliberti
<p>We’d like to thank Cooley and Fernandez-Perez for their thoughtful comments and feedback on our article. The Authors underline that using standard classification schemes of interstitial lung disease (ILD) clinical diagnoses, the number of unique ILDs is far from exceeding 200. Moreover, the Authors noticed that this number is frequently reported in several papers.</p><p>Depending on how you want to slice and dice it, the number of ILDs can vary broadly. Taxonomy requires determining whether to lump together entities in one category or split them apart [1]. The nosology of disease entities has historically relied on clinical and phenotypic features but other information has been progressively incorporated such as imaging, histology, biomarkers, and other data [2]. While phenotypic features may be relevant to the clinical diagnosis of a specific disease, they are not necessarily specific to the underlying cause. This is certainly true in some conditions that are considered to have a Mendelian pattern of inheritance. However, these conditions are rarely recognized in ILD.</p><p>It should be emphasized that the classification of ILD has deeply evolved over the last several decades, with increasing attention placed on the multidisciplinary integration of clinical features with radiological and pathological patterns [2]. Moreover, the results of recent trials have sparked the ongoing debate of whether to lump or split ILD patients based on their disease behavior, as in the case of progressive pulmonary fibrosis (PPF) [3]. As suggested by recent data, lumping PPF patients together simplifies ILD management and treatment [4]. On the other hand in the lumping spectrum, some ILDs are almost entirely dominated by lung inflammation. These ILDs are approached much differently in terms of both pharmacological and non-pharmacological interventions. Moreover, splitting specific ILDs into subgroups based on the improving understanding of disease biology has the advantage of distinguishing prognostic trajectories and potentially identifying new targeted therapies [5]. As an example, classifying pulmonary fibrosis (PF) as MUC5B-PF or telomeropathy-PF instead of using the word “idiopathic” might be a better approach to classify the disease based on its behavior [6]. Treating endotypes with targeted therapies based on the expression of specific biomarkers could maximize the effectiveness of existing or new therapies, such as the case of synthetic androgen danazol for patients with short telomeres or the use of N-Acetylcysteine based on TOLLIP gene variants in IPF patients [7, 8]. Thus, the splitting and the lumping approaches are not mutually exclusive. We believe that the ILD field will move to a dynamic disease classification in which treatment approaches will be governed not only by the classification based on etiologies, phenotypes and endotypes but also by the disease behavior [9]. In this context, a treatable traits approach could provide a comprehensive pat
走在间质性肺病可治疗性状的道路上。Respir Res. 2023;24(1):251. https://doi.org/10.1186/s12931-023-02554-8.Published 2023 Oct 24.Article PubMed PubMed Central Google Scholar Amati F, Spagnolo P, Oldham JM, et al.柳叶刀呼吸医学。https://doi.org/10.1016/S2213-2600(23)00002-4.Article PubMed Google Scholar Download referencesNot applicable.Not applicable.作者和单位意大利米兰，20072，Via Rita Levi Montalcini 4, Pieve Emanuele，Humanitas 大学生物医学科学系Francesco Amati, Anna Stainer & Stefano Aliberti意大利米兰，20089，Via Manzoni 56, Rozzano，IRCCS Humanitas 研究医院呼吸科Francesco Amati, Anna Stainer &；Stefano Aliberti作者弗朗西斯科-阿马蒂查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者安娜-斯泰纳查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者斯特凡诺-阿里贝尔蒂查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者供稿FA、AS和SA从一开始就参与了手稿的撰写，并阅读和批准了最终草案。所有作者均为论文的保证人，并对论文从开始到发表的整体完整性负责。伦理批准和参与同意不适用。同意发表本评论不包含任何个人的任何形式的数据。开放获取本文采用知识共享署名 4.0 国际许可协议进行许可，该协议允许以任何媒介或格式使用、共享、改编、分发和复制，只要您适当注明原作者和来源，提供知识共享许可协议的链接，并说明是否进行了修改。本文中的图片或其他第三方材料均包含在文章的知识共享许可协议中，除非在材料的署名栏中另有说明。如果材料未包含在文章的知识共享许可协议中，且您打算使用的材料不符合法律规定或超出许可使用范围，则您需要直接从版权所有者处获得许可。如需查看该许可的副本，请访问 http://creativecommons.org/licenses/by/4.0/。创意共享公共领域专用免责声明（http://creativecommons.org/publicdomain/zero/1.0/）适用于本文提供的数据，除非在数据的信用行中另有说明。转载与许可引用本文Amati, F., Stainer, A. & Aliberti, S. Response to: are there over 200 distinct types of interstitial lung diseases?Respir 25, 114 (2024). https://doi.org/10.1186/s12931-024-02751-zDownload citationReceived：21 February 2024Accepted: 27 February 2024Published: 06 March 2024DOI: https://doi.org/10.1186/s12931-024-02751-zShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative
{"title":"Response to: are there over 200 distinct types of interstitial lung diseases?","authors":"Francesco Amati, Anna Stainer, Stefano Aliberti","doi":"10.1186/s12931-024-02751-z","DOIUrl":"https://doi.org/10.1186/s12931-024-02751-z","url":null,"abstract":"<p>We’d like to thank Cooley and Fernandez-Perez for their thoughtful comments and feedback on our article. The Authors underline that using standard classification schemes of interstitial lung disease (ILD) clinical diagnoses, the number of unique ILDs is far from exceeding 200. Moreover, the Authors noticed that this number is frequently reported in several papers.</p><p>Depending on how you want to slice and dice it, the number of ILDs can vary broadly. Taxonomy requires determining whether to lump together entities in one category or split them apart [1]. The nosology of disease entities has historically relied on clinical and phenotypic features but other information has been progressively incorporated such as imaging, histology, biomarkers, and other data [2]. While phenotypic features may be relevant to the clinical diagnosis of a specific disease, they are not necessarily specific to the underlying cause. This is certainly true in some conditions that are considered to have a Mendelian pattern of inheritance. However, these conditions are rarely recognized in ILD.</p><p>It should be emphasized that the classification of ILD has deeply evolved over the last several decades, with increasing attention placed on the multidisciplinary integration of clinical features with radiological and pathological patterns [2]. Moreover, the results of recent trials have sparked the ongoing debate of whether to lump or split ILD patients based on their disease behavior, as in the case of progressive pulmonary fibrosis (PPF) [3]. As suggested by recent data, lumping PPF patients together simplifies ILD management and treatment [4]. On the other hand in the lumping spectrum, some ILDs are almost entirely dominated by lung inflammation. These ILDs are approached much differently in terms of both pharmacological and non-pharmacological interventions. Moreover, splitting specific ILDs into subgroups based on the improving understanding of disease biology has the advantage of distinguishing prognostic trajectories and potentially identifying new targeted therapies [5]. As an example, classifying pulmonary fibrosis (PF) as MUC5B-PF or telomeropathy-PF instead of using the word “idiopathic” might be a better approach to classify the disease based on its behavior [6]. Treating endotypes with targeted therapies based on the expression of specific biomarkers could maximize the effectiveness of existing or new therapies, such as the case of synthetic androgen danazol for patients with short telomeres or the use of N-Acetylcysteine based on TOLLIP gene variants in IPF patients [7, 8]. Thus, the splitting and the lumping approaches are not mutually exclusive. We believe that the ILD field will move to a dynamic disease classification in which treatment approaches will be governed not only by the classification based on etiologies, phenotypes and endotypes but also by the disease behavior [9]. In this context, a treatable traits approach could provide a comprehensive pat","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"30 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140047682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-06DOI: 10.1186/s12931-024-02731-3
Katharina Buschulte, Hans-Joachim Kabitz, Lars Hagmeyer, Peter Hammerl, Albert Esselmann, Conrad Wiederhold, Dirk Skowasch, Christoph Stolpe, Marcus Joest, Stefan Veitshans, Marc Höffgen, Phillen Maqhuzu, Larissa Schwarzkopf, Andreas Hellmann, Michael Pfeifer, Jürgen Behr, Rainer Karpavicius, Andreas Günther, Markus Polke, Philipp Höger, Vivien Somogyi, Christoph Lederer, Philipp Markart, Michael Kreuter
Interstitial lung diseases (ILD) comprise a heterogeneous group of mainly chronic lung diseases with different disease trajectories. Progression (PF-ILD) occurs in up to 50% of patients and is associated with increased mortality. The EXCITING-ILD (Exploring Clinical and Epidemiological Characteristics of Interstitial Lung Diseases) registry was analysed for disease trajectories in different ILD. The course of disease was classified as significant (absolute forced vital capacity FVC decline > 10%) or moderate progression (FVC decline 5–10%), stable disease (FVC decline or increase < 5%) or improvement (FVC increase ≥ 5%) during time in registry. A second definition for PF-ILD included absolute decline in FVC % predicted ≥ 10% within 24 months or ≥ 1 respiratory-related hospitalisation. Risk factors for progression were determined by Cox proportional-hazard models and by logistic regression with forward selection. Kaplan-Meier curves were utilised to estimate survival time and time to progression. Within the EXCITING-ILD registry 28.5% of the patients died (n = 171), mainly due to ILD (n = 71, 41.5%). Median survival time from date of diagnosis on was 15.5 years (range 0.1 to 34.4 years). From 601 included patients, progression was detected in 50.6% of the patients (n = 304) with shortest median time to progression in idiopathic NSIP (iNSIP; median 14.6 months) and idiopathic pulmonary fibrosis (IPF; median 18.9 months). Reasons for the determination as PF-ILD were mainly deterioration in lung function (PFT; 57.8%) and respiratory hospitalisations (40.6%). In multivariate analyses reduced baseline FVC together with age were significant predictors for progression (OR = 1.00, p < 0.001). Higher GAP indices were a significant risk factor for a shorter survival time (GAP stage III vs. I HR = 9.06, p < 0.001). A significant shorter survival time was found in IPF compared to sarcoidosis (HR = 0.04, p < 0.001), CTD-ILD (HR = 0.33, p < 0.001), and HP (HR = 0.30, p < 0.001). Patients with at least one reported ILD exacerbation as a reason for hospitalisation had a median survival time of 7.3 years (range 0.1 to 34.4 years) compared to 19.6 years (range 0.3 to 19.6 years) in patients without exacerbations (HR = 0.39, p < 0.001). Disease progression is common in all ILD and associated with increased mortality. Most important risk factors for progression are impaired baseline forced vital capacity and higher age, as well as acute exacerbations and respiratory hospitalisations for mortality. Early detection of progression remains challenging, further clinical criteria in addition to PFT might be helpful.
{"title":"Disease trajectories in interstitial lung diseases – data from the EXCITING-ILD registry","authors":"Katharina Buschulte, Hans-Joachim Kabitz, Lars Hagmeyer, Peter Hammerl, Albert Esselmann, Conrad Wiederhold, Dirk Skowasch, Christoph Stolpe, Marcus Joest, Stefan Veitshans, Marc Höffgen, Phillen Maqhuzu, Larissa Schwarzkopf, Andreas Hellmann, Michael Pfeifer, Jürgen Behr, Rainer Karpavicius, Andreas Günther, Markus Polke, Philipp Höger, Vivien Somogyi, Christoph Lederer, Philipp Markart, Michael Kreuter","doi":"10.1186/s12931-024-02731-3","DOIUrl":"https://doi.org/10.1186/s12931-024-02731-3","url":null,"abstract":"Interstitial lung diseases (ILD) comprise a heterogeneous group of mainly chronic lung diseases with different disease trajectories. Progression (PF-ILD) occurs in up to 50% of patients and is associated with increased mortality. The EXCITING-ILD (Exploring Clinical and Epidemiological Characteristics of Interstitial Lung Diseases) registry was analysed for disease trajectories in different ILD. The course of disease was classified as significant (absolute forced vital capacity FVC decline > 10%) or moderate progression (FVC decline 5–10%), stable disease (FVC decline or increase < 5%) or improvement (FVC increase ≥ 5%) during time in registry. A second definition for PF-ILD included absolute decline in FVC % predicted ≥ 10% within 24 months or ≥ 1 respiratory-related hospitalisation. Risk factors for progression were determined by Cox proportional-hazard models and by logistic regression with forward selection. Kaplan-Meier curves were utilised to estimate survival time and time to progression. Within the EXCITING-ILD registry 28.5% of the patients died (n = 171), mainly due to ILD (n = 71, 41.5%). Median survival time from date of diagnosis on was 15.5 years (range 0.1 to 34.4 years). From 601 included patients, progression was detected in 50.6% of the patients (n = 304) with shortest median time to progression in idiopathic NSIP (iNSIP; median 14.6 months) and idiopathic pulmonary fibrosis (IPF; median 18.9 months). Reasons for the determination as PF-ILD were mainly deterioration in lung function (PFT; 57.8%) and respiratory hospitalisations (40.6%). In multivariate analyses reduced baseline FVC together with age were significant predictors for progression (OR = 1.00, p < 0.001). Higher GAP indices were a significant risk factor for a shorter survival time (GAP stage III vs. I HR = 9.06, p < 0.001). A significant shorter survival time was found in IPF compared to sarcoidosis (HR = 0.04, p < 0.001), CTD-ILD (HR = 0.33, p < 0.001), and HP (HR = 0.30, p < 0.001). Patients with at least one reported ILD exacerbation as a reason for hospitalisation had a median survival time of 7.3 years (range 0.1 to 34.4 years) compared to 19.6 years (range 0.3 to 19.6 years) in patients without exacerbations (HR = 0.39, p < 0.001). Disease progression is common in all ILD and associated with increased mortality. Most important risk factors for progression are impaired baseline forced vital capacity and higher age, as well as acute exacerbations and respiratory hospitalisations for mortality. Early detection of progression remains challenging, further clinical criteria in addition to PFT might be helpful.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"3 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140047811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-05DOI: 10.1186/s12931-024-02744-y
Nika Elmi, Yasmin Sadri, Frank Myslik, Jordan Chenkin, William Cherniak
Access to timely and accurate diagnostic imaging is essential for high-quality healthcare. Point-of-care ultrasound has been shown to be accessible and effective in many aspects of healthcare, including assessing changes in lung pathology. However, few studies have examined self-administered at-home lung ultrasound (SAAH-LUS), in particular performed by non-clinical patients (NCPs). Are NCPs able to perform SAAH-LUS using remote teleguidance and produce interpretable images? Patients were enrolled to the study in a mix of in-person and virtual recruitment, and shipped a smartphone as well as a point of care ultrasound device. Tele-guidance was provided by a remote physician using software integrated with the point of care ultrasound device, allowing real-time remote visualization and guidance of a patient scanning their own chest. A post-intervention survey was conducted to assess patient satisfaction, feasibility, and acceptability of SAAH-LUS. Two POCUS expert reviewers reviewed the scans for interpretability, and inter-rater agreement between the two reviewers was also computed. Eighteen patients successfully underwent 7–14 days of daily telemedicine in parallel to daily SAAH-LUS. Across 1339 scans obtained from ten different lung zones, the average proportion of interpretability was 96% with a chance-corrected agreement, or Cohen’s kappa, reported as κ = 0.67 (significant agreement). 100% of NCPs surveyed found SAAH-LUS to be a positive experience, particularly for its ease of operation and ability to increase access to healthcare services. This study demonstrates that NCPs can obtain interpretable LUS images at home, highlighting the potential for SAAH-LUS to increase diagnostic capacity, particularly for rural and remote regions where complex imaging and healthcare providers are difficult to obtain. Trial registration The clinical trials has been registered (clinicaltrials.gov). Registration number: NCT04967729
{"title":"Self-administered at-home lung ultrasound with remote guidance in patients without clinical training","authors":"Nika Elmi, Yasmin Sadri, Frank Myslik, Jordan Chenkin, William Cherniak","doi":"10.1186/s12931-024-02744-y","DOIUrl":"https://doi.org/10.1186/s12931-024-02744-y","url":null,"abstract":"Access to timely and accurate diagnostic imaging is essential for high-quality healthcare. Point-of-care ultrasound has been shown to be accessible and effective in many aspects of healthcare, including assessing changes in lung pathology. However, few studies have examined self-administered at-home lung ultrasound (SAAH-LUS), in particular performed by non-clinical patients (NCPs). Are NCPs able to perform SAAH-LUS using remote teleguidance and produce interpretable images? Patients were enrolled to the study in a mix of in-person and virtual recruitment, and shipped a smartphone as well as a point of care ultrasound device. Tele-guidance was provided by a remote physician using software integrated with the point of care ultrasound device, allowing real-time remote visualization and guidance of a patient scanning their own chest. A post-intervention survey was conducted to assess patient satisfaction, feasibility, and acceptability of SAAH-LUS. Two POCUS expert reviewers reviewed the scans for interpretability, and inter-rater agreement between the two reviewers was also computed. Eighteen patients successfully underwent 7–14 days of daily telemedicine in parallel to daily SAAH-LUS. Across 1339 scans obtained from ten different lung zones, the average proportion of interpretability was 96% with a chance-corrected agreement, or Cohen’s kappa, reported as κ = 0.67 (significant agreement). 100% of NCPs surveyed found SAAH-LUS to be a positive experience, particularly for its ease of operation and ability to increase access to healthcare services. This study demonstrates that NCPs can obtain interpretable LUS images at home, highlighting the potential for SAAH-LUS to increase diagnostic capacity, particularly for rural and remote regions where complex imaging and healthcare providers are difficult to obtain. Trial registration The clinical trials has been registered (clinicaltrials.gov). Registration number: NCT04967729","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"14 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140037731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acute lung injury (ALI) is one of the life-threatening complications of sepsis, and macrophage polarization plays a crucial role in the sepsis-associated ALI. However, the regulatory mechanisms of macrophage polarization in ALI and in the development of inflammation are largely unknown. In this study, we demonstrated that macrophage polarization occurs in sepsis-associated ALI and is accompanied by mitochondrial dysfunction and inflammation, and a decrease of PRDX3 promotes the initiation of macrophage polarization and mitochondrial dysfunction. Mechanistically, PRDX3 overexpression promotes M1 macrophages to differentiate into M2 macrophages, and enhances mitochondrial functional recovery after injury by reducing the level of glycolysis and increasing TCA cycle activity. In conclusion, we identified PRDX3 as a critical hub integrating oxidative stress, inflammation, and metabolic reprogramming in macrophage polarization. The findings illustrate an adaptive mechanism underlying the link between macrophage polarization and sepsis-associated ALI.
急性肺损伤（ALI）是脓毒症危及生命的并发症之一，巨噬细胞极化在脓毒症相关的急性肺损伤中起着至关重要的作用。然而，巨噬细胞极化在 ALI 和炎症发展过程中的调控机制尚不清楚。本研究表明，巨噬细胞极化发生在脓毒症相关的 ALI 中，并伴随线粒体功能障碍和炎症，而 PRDX3 的减少会促进巨噬细胞极化和线粒体功能障碍的启动。从机制上讲，PRDX3 过表达可促进 M1 巨噬细胞分化为 M2 巨噬细胞，并通过降低糖酵解水平和提高 TCA 循环活性来增强损伤后线粒体功能的恢复。总之，我们发现 PRDX3 是巨噬细胞极化过程中整合氧化应激、炎症和代谢重编程的关键枢纽。这些发现说明了巨噬细胞极化与脓毒症相关 ALI 之间的适应性机制。
{"title":"Peroxiredoxin 3 has a crucial role in the macrophage polarization by regulating mitochondrial homeostasis","authors":"Wenhui Huang, Lianfang Wang, Zhipeng Huang, Zhichao Sun, Bojun Zheng","doi":"10.1186/s12931-024-02739-9","DOIUrl":"https://doi.org/10.1186/s12931-024-02739-9","url":null,"abstract":"Acute lung injury (ALI) is one of the life-threatening complications of sepsis, and macrophage polarization plays a crucial role in the sepsis-associated ALI. However, the regulatory mechanisms of macrophage polarization in ALI and in the development of inflammation are largely unknown. In this study, we demonstrated that macrophage polarization occurs in sepsis-associated ALI and is accompanied by mitochondrial dysfunction and inflammation, and a decrease of PRDX3 promotes the initiation of macrophage polarization and mitochondrial dysfunction. Mechanistically, PRDX3 overexpression promotes M1 macrophages to differentiate into M2 macrophages, and enhances mitochondrial functional recovery after injury by reducing the level of glycolysis and increasing TCA cycle activity. In conclusion, we identified PRDX3 as a critical hub integrating oxidative stress, inflammation, and metabolic reprogramming in macrophage polarization. The findings illustrate an adaptive mechanism underlying the link between macrophage polarization and sepsis-associated ALI.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"34 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140017950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01DOI: 10.1186/s12931-024-02671-y
Dong-gon Hyun, Su Yeon Lee, Jee Hwan Ahn, Sang-Bum Hong, Chae-Man Lim, Younsuck Koh, Jin Won Huh
There is an argument whether the delayed intubation aggravate the respiratory failure in Acute respiratory distress syndrome (ARDS) patients with coronavirus disease 2019 (COVID-19). We aimed to investigate the effect of high-flow nasal cannula (HFNC) failure before mechanical ventilation on clinical outcomes in mechanically ventilated patients with COVID-19. This retrospective cohort study included mechanically ventilated patients who were diagnosed with COVID-19 and admitted to the intensive care unit (ICU) between February 2020 and December 2021 at Asan Medical Center. The patients were divided into HFNC failure (HFNC-F) and mechanical ventilation (MV) groups according to the use of HFNC before MV. The primary outcome of this study was to compare the worst values of ventilator parameters from day 1 to day 3 after mechanical ventilation between the two groups. Overall, 158 mechanically ventilated patients with COVID-19 were included in this study: 107 patients (67.7%) in the HFNC-F group and 51 (32.3%) in the MV group. The two groups had similar profiles of ventilator parameter from day 1 to day 3 after mechanical ventilation, except of dynamic compliance on day 3 (28.38 mL/cmH2O in MV vs. 30.67 mL/H2O in HFNC-F, p = 0.032). In addition, the HFNC-F group (5.6%) had a lower rate of ECMO at 28 days than the MV group (17.6%), even after adjustment (adjusted hazard ratio, 0.30; 95% confidence interval, 0.11–0.83; p = 0.045). Among mechanically ventilated COVID-19 patients, HFNC failure before mechanical ventilation was not associated with deterioration of respiratory failure.
{"title":"Prognosis of mechanically ventilated patients with COVID-19 after failure of high-flow nasal cannula: a retrospective cohort study","authors":"Dong-gon Hyun, Su Yeon Lee, Jee Hwan Ahn, Sang-Bum Hong, Chae-Man Lim, Younsuck Koh, Jin Won Huh","doi":"10.1186/s12931-024-02671-y","DOIUrl":"https://doi.org/10.1186/s12931-024-02671-y","url":null,"abstract":"There is an argument whether the delayed intubation aggravate the respiratory failure in Acute respiratory distress syndrome (ARDS) patients with coronavirus disease 2019 (COVID-19). We aimed to investigate the effect of high-flow nasal cannula (HFNC) failure before mechanical ventilation on clinical outcomes in mechanically ventilated patients with COVID-19. This retrospective cohort study included mechanically ventilated patients who were diagnosed with COVID-19 and admitted to the intensive care unit (ICU) between February 2020 and December 2021 at Asan Medical Center. The patients were divided into HFNC failure (HFNC-F) and mechanical ventilation (MV) groups according to the use of HFNC before MV. The primary outcome of this study was to compare the worst values of ventilator parameters from day 1 to day 3 after mechanical ventilation between the two groups. Overall, 158 mechanically ventilated patients with COVID-19 were included in this study: 107 patients (67.7%) in the HFNC-F group and 51 (32.3%) in the MV group. The two groups had similar profiles of ventilator parameter from day 1 to day 3 after mechanical ventilation, except of dynamic compliance on day 3 (28.38 mL/cmH2O in MV vs. 30.67 mL/H2O in HFNC-F, p = 0.032). In addition, the HFNC-F group (5.6%) had a lower rate of ECMO at 28 days than the MV group (17.6%), even after adjustment (adjusted hazard ratio, 0.30; 95% confidence interval, 0.11–0.83; p = 0.045). Among mechanically ventilated COVID-19 patients, HFNC failure before mechanical ventilation was not associated with deterioration of respiratory failure.","PeriodicalId":21109,"journal":{"name":"Respiratory Research","volume":"7 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140003745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：