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It is estimated that there are 544.9 million people suffering from chronic respiratory diseases in the world, which is the third largest chronic disease. Although there are various clinical treatment methods, there is no specific drug for chronic pulmonary diseases, including chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD) and idiopathic pulmonary fibrosis (IPF). Therefore, it is urgent to clarify the pathological mechanism and medication development. Single-cell transcriptome data of human and mouse from GEO database were integrated by "Harmony" algorithm. The data was standardized and normalized by using "Seurat" package, and "SingleR" algorithm was used for cell grouping annotation. The "Findmarker" function is used to find differentially expressed genes (DEGs), which were enriched and analyzed by using "clusterProfiler", and a protein interaction network was constructed for DEGs, and four algorithms are used to find the hub genes. The expression of hub genes were analyzed in independent human and mouse single-cell transcriptome data. Bulk RNA data were used to integrate by the "SVA" function, verify the expression levels of hub genes and build a diagnostic model. The L1000FWD platform was used to screen potential drugs. Through exploring the similarities and differences by integrated single-cell atlas, we found that the lung parenchymal cells showed abnormal oxidative stress, cell matrix adhesion and ubiquitination in COPD, corona virus disease 2019 (COVID-19), ILD and IPF. Meanwhile, the lung resident immune cells showed abnormal Toll-like receptor signals, interferon signals and ubiquitination. However, unlike acute pneumonia (COVID-19), chronic pulmonary disease shows enhanced ubiquitination. This phenomenon was confirmed in independent external human single-cell atlas, but unfortunately, it was not confirmed in mouse single-cell atlas of bleomycin-induced pulmonary fibrosis model and influenza virus-infected mouse model, which means that the model needs to be optimized. In addition, the bulk RNA-Seq data of COVID-19, ILD and IPF was integrated, and we found that the immune infiltration of lung tissue was enhanced, consistent with the single-cell level, UBA52, UBB and UBC were low expressed in COVID-19 and high expressed in ILD, and had a strong correlation with the expression of cell matrix adhesion genes. UBA52 and UBB have good diagnostic efficacy, and salermide and SSR-69071 can be used as their candidate drugs. Our study found that the disorder of protein ubiquitination in chronic pulmonary diseases is an important cause of pathological phenotype of pulmonary fibrosis by integrating scRNA-Seq and bulk RNA-Seq, which provides a new horizons for clinicopathology, diagnosis and treatment.

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The lungs, as vital organs in the human body, continuously engage in gas exchange with the external environment. The lung microbiota, a critical component in maintaining internal homeostasis, significantly influences the onset and progression of diseases. Beneficial interactions between the host and its microbial community are essential for preserving the host's health, whereas disease development is often linked to dysbiosis or alterations in the microbial community. Evidence has demonstrated that changes in lung microbiota contribute to the development of major chronic lung diseases, including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), asthma, and lung cancer. However, in-depth mechanistic studies are constrained by the small scale of the lung microbiota and its susceptibility to environmental pollutants and other factors, leaving many questions unanswered. This review examines recent research on the lung microbiota and lung diseases, as well as methodological advancements in studying lung microbiota, summarizing the ways in which lung microbiota impacts lung diseases and introducing research methods for investigating lung microbiota.

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Acupuncture treatment in local areas is commonly used to treat pain or soreness; however, acupuncture around the neck or shoulder may be a risk factor for pneumothorax. Herein, we report two cases of iatrogenic pneumothorax after acupuncture. These points indicate that physicians should be aware of these risk factors through history-taking before acupuncture. Chronic pulmonary diseases, such as chronic bronchitis, emphysema, tuberculosis, lung cancer, pneumonia, and thoracic surgery, may be associated with a higher risk of iatrogenic pneumothorax after acupuncture. Even if the incidence of pneumothorax should be low under caution and fully evaluated, it is still recommended to arrange further imaging examinations to rule out the possibility of iatrogenic pneumothorax.

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Genetic information is not transmitted solely by DNA but by the epigenetics process. Epigenetics describes molecular missing link pathways that could bridge the gap between the genetic background and environmental risk factors that contribute to the pathogenesis of pulmonary fibrosis. Specific epigenetic patterns, especially DNA methylation, histone modifications, long non-coding, and microRNA (miRNAs), affect the endophenotypes underlying the development of idiopathic pulmonary fibrosis (IPF). Among all the epigenetic marks, DNA methylation modifications have been the most widely studied in IPF. This review summarizes the current knowledge concerning DNA methylation changes in pulmonary fibrosis and demonstrates a promising novel epigenetics-based precision medicine.

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Rationale: Telemedicine consults, including video consults, telephone consults, electronic consults, and virtual conferences, may be particularly valuable in the management of chronic pulmonary diseases, but there is limited guidance on best practices for pulmonary telemedicine consults. Objectives: This scoping review aims to identify, characterize, and analyze gaps in the published literature on telemedicine consults health providers use to manage patients with chronic pulmonary diseases. Methods: We searched PubMed, Embase, Web of Science, and Cochrane Library from database origin through July 10, 2021. We included manuscripts describing applications of telemedicine consults for patients with chronic pulmonary diseases (asthma, chronic obstructive pulmonary disease, lung cancer, pulmonary hypertension, and interstitial lung disease). We restricted our review to full-length articles published in English about provider-led (as opposed to nurse-led) telemedicine consults. Results: Our search yielded 3,118 unique articles; 27 articles met the inclusion criteria. All telemedicine consult modalities and chronic pulmonary conditions were well represented in the review except for pulmonary hypertension and interstitial lung disease, which were represented by one and no articles, respectively. Most articles described a small, single-center, observational study that focused on the acceptability, feasibility, use, and/or clinical effectiveness of the telemedicine consult. Few studies had objectively measured clinical outcomes or included a comparator group, and none compared telemedicine consult modalities against one another. Conclusions: Our scoping review identified limited literature describing pulmonary telemedicine consults and highlighted several gaps in the literature that warrant increased attention. Providers treating chronic pulmonary diseases are left with limited guidance on best practices for telemedicine consults.

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Bronchial epithelial cells (BEC) play a crucial role in innate immunity against inhaled fungi. Indeed, in response to microorganisms, BEC synthesize proinflammatory cytokines involved in the recruitment of neutrophils. We have recently shown that BEC exert antifungal activity against Aspergillus fumigatus by inhibiting filament growth. In the present study, we first analyzed the inflammatory and antifungal responses of BEC infected by several fungal species such as Aspergillus spp., Scedosporium apiospermum and Candida albicans, which are frequently isolated from the sputum of people with chronic pulmonary diseases. The airways of these patients, such as people with cystic fibrosis (pwCF), are mainly colonized by P. aeruginosa and secondary by fungal pathogens. We have previously demonstrated that BEC are capable of innate immune memory, allowing them to increase their inflammatory response against A. fumigatus following a previous contact with Pseudomonas aeruginosa flagellin. To identify the impact of bacteria exposure on BEC responses to other fungal infections, we extended the analysis of BEC innate immune memory to Aspergillus spp., Scedosporium apiospermum and Candida albicans infection. Our results show that BEC are able to recognize and respond to Aspergillus spp., S. apiospermum and C. albicans infection and that the modulation of BEC responses by pre-exposure to flagellin varies according to the fungal species encountered. Deepening our knowledge of the innate immune memory of BEC should open new therapeutic avenues to modulate the inflammatory response against polymicrobial infections observed in chronic pulmonary diseases such as CF.

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Locomotor skeletal muscle dysfunction is a relevant comorbidity of chronic obstructive pulmonary disease (COPD) and is strongly associated with worse clinical outcomes including higher mortality. Over the last decades, a large body of literature helped characterize the process, defining the disruptive muscle phenotype caused by COPD that involves reduction in muscle mass, force-generation capacity, fatigue-tolerance, and regenerative potential following injury. A major limitation in the field has been the scarcity of well-calibrated animal models to conduct mechanistic research based on loss- and gain-of-function studies. This article provides an overall description of the process, the tools available to mechanistically investigate it, and the potential role of mitochondrially driven metabolic signals on the regulation muscle regeneration after injury in COPD. Finally, a description of future avenues to further expand on the area is proposed based on very recent evidence involving mitochondrial metabolic cues affecting myogenesis.

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Background: The coronavirus disease 19 (COVID-19) pandemic has spread rapidly around the globe with considerable morbidity and mortality. Coexistence of comorbidities with COVID-19 had consistently been reported as risk factors for unfavorable outcome. We aimed to evaluate the impact of comorbidities in COVID-19 patients on the outcome and determine predictors of prolonged hospital stay, requisite for intensive care unit (ICU) admission. Four hundred and thirty-nine adult patients who are admitted through (June and July 2020) in our University Hospitals were included in the study. All participants were diagnosed with COVID-19 according to Egyptian Ministry of Health guidance as definite case or probable case. Results: Patients with comorbidities represented 61.7% of all cases. Constitutional symptoms especially myalgia and lower respiratory tract (LRT) symptoms such as dyspnea were significantly higher in patients with comorbidities (P < 0.05). Patients with comorbidities had significantly worse laboratory parameters. ICU admission was higher in patients with comorbidities (35.8%). Among different comorbidities 45.4% of cardiovascular diseases (CVD) cases were admitted in ICU followed by diabetes mellitus (DM) cases (40.8%). Also, patients with comorbidities needed invasive mechanical ventilation more than those without comorbidity (31 versus 10.7%, P < 0.001). Significant lower frequency of recovery was found in COVID-19 patients with comorbidities (59% versus 81%, P < 0.001) and death rate was significantly higher in cases with comorbidities (P < 0.001) . The survival rates in cases with pre-existing CVD and neurological diseases were lower than those without disease (P < 0.002 and 0.001, respectively). Conclusions: Association of cardiovascular comorbid conditions including hypertension or neurological diseases including old cerebrovascular strokes together with COVID-19 infections carries higher risks of mortality. However, other comorbidities such as diabetes mellitus, chronic pulmonary or kidney diseases may also contribute to increased COVID-19 severity.

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BACKGROUND: This study aimed to validate the Korean version of the Patient-Reported Outcome Measurement Information System 29 Profile V2.1 (K-PROMIS-29 V2.1) in a sample of patients with chronic pulmonary diseases (CPDs). METHODS: Participants were recruited from the respiratory disease outpatient clinics of Samsung Medical Center in Seoul, South Korea, from September to October 2018. Participants completed a survey questionnaire, including the K-PROMIS-29 V2.1 and Short Form Health Survey version-2.0 (SF-36v2). Modified Medical Research Council (mMRC) and chronic obstructive pulmonary disease (COPD) Assessment Test (CAT) scores were obtained these scores from electronic medical records (EMRs). Exploratory and confirmatory factor analyses (CFA) and Pearson's correlations were used to evaluate the reliability and validity of the K-PROMIS-29 V2.1. RESULTS: The mean age [standard deviation (SD)] was 62.8 (12.0) years, and 19.2% had less than middle-school education. Disease types included bronchiectasis (n=46, 24.5%), COPD (n=45, 23.9%), nontuberculous mycobacterial lung disease (n=25, 13.3%), interstitial lung disease (n=22, 11.7%), and others (n=50, 26.6%). Cronbach's alpha coefficients of the 7 subdomains in the K-PROMIS-29 V2.1 ranged from 0.77 to 0.96, indicating satisfactory internal consistency. In CFA, the goodness-of-fit indices were high (comparative fit index =0.90, standardised root mean residual =0.06). Moderate correlations were observed between comparable subscales of the K-PROMIS-29 V2.1 and those of the SF-36v2 (r=0.55-0.70) and CAT (r=-0.80 to 0.70). CONCLUSIONS: The findings of this study suggest that the K-PROMIS-29 V2.1 is a reliable and valid measure for assessing a broad range of health-related quality-of-life domains in patients with CPDs.

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BACKGROUND: Patients with pulmonary diseases often experience fatigue. Severe fatigue is associated with a worse health status and worse physical and social functioning. The study aimed to evaluate the relationship between fatigue and quality of life in patients with nonmalignant pulmonary diseases. METHODS: The St George's Respiratory Questionnaire (SGRQ) was used to assess health status and the Fatigue Impact Scale (MFIS) to measure the level of fatigue. The Shapiro-Wilk test was used to test for normal distribution. Correlations were described as Spearman's rank correlation coefficient. RESULTS: The study included 200 consecutive patients (mean age, 57.7) with the following diagnoses: COPD (26%), asthma (36%), obstructive sleep apnoea (19%), pneumonia or bronchitis of various aetiologies (8.5%), bronchiectasis (2.5%), interstitial lung disease (3%). The mean score in the SGRQ was 44.62 ± 24.94. The mean score in the MFIS was 28.64 ± 15.8. The strongest correlations appeared between quality-of-life scales and fatigue as measured by physical functioning (symptoms r = 0.622; activity r = 0.632; impact r = 0.692; p < 0.001 for all subscales); however, all the correlations between SGRQ and MFIS were significant. CONCLUSIONS: Patients with chronic pulmonary diseases were revealed to have a reduced level of quality of life and an increased level of fatigue. The negative influence of fatigue on quality of life highlights the need for careful and routine assessment of this symptom in pulmonary patients. Treating fatigue may improve quality of life and increase the ability of patients with chronic pulmonary diseases to perform activities in daily life.

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Recalcitrant respiratory tract infections caused by bacteria have emerged as one of the greatest health challenges worldwide. Aerosolized antimicrobial therapy is becoming increasingly attractive to combat such infections, as it allows targeted delivery of high drug concentrations to the infected organ while limiting systemic exposure. However, successful aerosolized antimicrobial therapy is still challenged by the diverse biological barriers in infected lungs. Nanoparticle-mediated pulmonary drug delivery is gaining increasing attention as a means to overcome the biological barriers and accomplish site-specific drug delivery by controlling release of the loaded drug(s) at the target site. With the aim to summarize emerging efforts in combating respiratory tract infections by using nanoparticle-mediated pulmonary delivery strategies, this review provides a brief introduction to the bacterial infection-related pulmonary diseases and the biological barriers for effective treatment of recalcitrant respiratory tract infections. This is followed by a summary of recent advances in design of inhalable nanoparticle-based drug delivery systems that overcome the biological barriers and increase drug bioavailability. Finally, challenges for the translation from exploratory laboratory research to clinical application are also discussed and potential solutions proposed.

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Chronic obstructive respiratory disorders such as asthma and chronic obstructive pulmonary disease (COPD) have their roots in the womb. Together with a genetic predisposition, prenatal and early-life factors, including maternal smoking, prematurity, and bronchopulmonary dysplasia (BPD), have a pivotal role in later respiratory health. Then, inappropriate responses to respiratory viruses (especially respiratory syncytial virus and rhinovirus) and early allergic sensitization are the strongest contributors to the inception of wheezing and early-onset asthma. There is an urgent need for early disease biomarkers to identify profiles at higher risk of chronic respiratory conditions. Applying the "-omic" technologies to urine, blood and breath condensate, and non-invasive inflammometry seem promising in this regard. The description of specific risk profiles may be the key to the use of targeted personalized therapies.

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BACKGROUND: The objective was to screen and evaluate the prevalence of respiratory diseases and obstructive ventilatory defects among fishermen in Morocco. MATERIALS AND METHODS: This observational and cross-sectional epidemiological study involved 924 men over 20 years old and with at least two years of seniority. It included a questionnaire and a spirometry. The questionnaire is composed of four sections: sociodemographic and occupational characteristics, toxic habits, medical history and respiratory clinical symptoms. RESULTS: The prevalence of symptoms of tracheobronchial irritation was 9.2% for cough, 8.2% for sputum 7.8% for dyspnoea and chest wheezing 8.1%. The frequency of rhinitis was 17.1%, asthma 6.8%, chronic bronchitis 5.6% and chronic obstructive pulmonary disease (COPD) 4.1% (5.4% for current and former smokers versus 1.1% for non-smokers). The prevalence was reaching 6.8% among those who smoked more than 10 pack-years and 17.9% among those who smoked more than 20 pack-years. Among subjects over 40 years old who had smoked more than 10 pack-years, the prevalence of COPD was 8.1%. The comorbidities were frequent. CONCLUSIONS: Smoking was very common among fishermen. Symptoms and respiratory diseases remain underdiagnosed and undertreated. Prevention and early detection must be a priority in this sector.

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Objective To assess the value of serum amyloid A(SAA)in patients with acute exacerbation of chronic pulmonary diseases. Methods Seventy AECOPD patients were randomly chosen. The AECOPD patients were divided into bacterial infection induced group and non-bacterial infection induced group by sputum bacteria culture. Thirty five SCOPD patients were chosen as control group. General data was collected. Lung function ,chest X ray,blood routine,CRP,SAA,IL6 and PCT were deteced and compared in the 3 groups. The diagnostic value of SAA to distinguish bacterial infection induced AECOPD was estimated. Results SAA of both AECOPD sub-groups were significantly higher than that of healthy controls. SAA in infection group is higher that that in exacerba-tion group. In terms of ROC curve,AUC was 0.8682 for SAA to distinguish merging bacterial infection,and the cut-off value was 72.10 mg/L with sensitivity of 94.29% and specificity of 65.71%. Conclusion SAA increases in AECOPD patients,and more obviously in AECOPD patients with bacterial infection. SAA may be used as a reliable biomarker not only to distinguish AECOPD patients from SCOPD patients ,but also distinguish merging bacterial infection during AECOPD.

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BACKGROUND: The detection of Pneumocystis jirovecii DNA in respiratory specimen from individuals who do not have signs or symptoms of pneumonia has been defined as colonization. The role of P. jirovecii colonization in the development or progression of various lung diseases has been reported, but little information about P. jirovecii colonization in patients is available in the People's Republic of China. OBJECTIVE: To determine the prevalence of P. jirovecii colonization in patients with various pulmonary diseases, including the acute and stable stage of COPD, interstitial lung diseases, cystic fibrosis, and chronic bronchiectasis. MATERIALS AND METHODS: A loop-mediated isothermal amplification (LAMP) and a conventional polymerase chain reaction (PCR) method for detecting P. jirovecii were developed. Ninety-eight HIV-negative patients who were followed-up and who had undergone bronchoscopy for diagnosis of various underlying respiratory diseases were included in the study. Sputa of these patients were analyzed with LAMP amplification of P. jirovecii gene. In addition, conventional PCR, Giemsa and Gomori's methenamine silver nitrate staining assays were applied to all specimens. RESULTS: The sensitivity and specificity test showed that there was no cross-reaction with other fungi or bacteria in detecting the specific gene of P. jirovecii by LAMP, and the minimum detection limits by LAMP was 50 copies/mL. P. jirovecii DNA was detected in 62 of 98 (63.3%) sputa specimens by LAMP assay and 22.45% (22/98) by conventional PCR. However, no P. jirovecii cysts were found by Giemsa and Gomori's methenamine silver nitrate in all of gene-positive specimens. CONCLUSION: The results of our study showed that prevalence of P. jirovecii colonization is particularly high in patients with chronic pulmonary diseases in the People's Republic of China, and the LAMP method is better for evaluation of the colonization of P. jirovecii in sputum specimen than conventional PCR.

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Chronic pulmonary diseases represent a segment of pathology with an increasing prevalence worldwide, this requiring joint efforts from specialists in this field to (a) identify those factors insufficiently explored so far, but critical for their evolution and (b) address them via new therapies. This study aims to explore the existing data regarding the psychological factors involved in the dynamics of chronic pulmonary diseases and the main possibilities of psychological intervention, as a distinct part of pulmonary rehabilitation (PR). 49 articles published on this topic in peer-reviewed journals between 1979 and 2010, indexed in PubMed, ProQuest and EBSCO databases, were examined for evidence. Among psychological factors considered important by study authors were the following: 1) the deficient instruction of the patient, 2) decreased treatment motivation, 3) a marginal social role, 4) a disadaptive cognitive style and 5) psychiatric comorbidity (especially anxiety and depression). Efficient interventions were, for physicians, 1) patient education and 2) designing a personalized self-management plan, and for the clinical psychologists, 1) cognitive-behavioral therapy, 2) biofeedback, 3) family therapy, 4) relaxation and 5) hypnosis. Despite the undeniable effect of these methods in selected cases, the high heterogeneity of designs and personal affiliations of researchers do not allow new generalizations about their efficacy or their routine implementation into PR. Further research including larger samples, more uniform designs, construction of consensual international standards regarding the objectives of PR, and assessments done by experts from multiple study domains could contribute to a better understanding of the role psychological interventions could play in PR.

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The most important long-term complication of pulmonary thromboembolism is chronic thromboembolic pulmonary hypertension (CTEPH) that is associated with considerable morbidity and mortality. It is uncertain why some patients with acute pulmonary embolism (PE) develop CTEPH and others do not. Elevated red cell distribution width (RDW) has been associated with adverse outcomes of heart failure, PE, and idiopathic pulmonary hypertension. The aim of the present study was to investigate whether RDW might be a predictor of CTEPH in PE patients or not. This study is a retrospective cohort study. A total of 203 consecutive patients with acute PE were included. The RDW was higher in the CTEPH patients than the patients without CTEPH (17.04 ± 3.46, 14.64 ± 1.82, respectively, p = 0.015). RDW was also higher in the CTEPH patients at the time of diagnosis of CTEPH during follow-up compared with the baseline RDW level at the time of PE diagnosis (18.63 ± 3.58, 17.02 ± 3.59, respectively, p = 0.014). The optimal cutoff value of the RDW for predicting CTEPH was 14.65. The area under the curve of RDW for the prediction of CTEPH was 0.735 (95% confidence interval (CI): 0.600-0.869); in cases with RDW levels >14.65%, the specificity, sensitivity, and negative predictive value for CTEPH were 62% (95% CI: 0.55-0.69), 75% (95% CI: 0.47-0.92), and 96.7% (95% CI: 0.91-0.99), respectively. A multivariate regression analysis showed that RDW, hazard ratio: 1.58 (95% CI: 1.09-2.30), was a predictor of CTEPH (p = 0.016). High level of RDW was an independent predictor of CTEPH in PE patients. Therefore, RDW levels may provide a prediction for CTEPH in PE patients.

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In the last few decades, aerially transmitted human fungal pathogens have been increasingly recognized to impact the clinical course of chronic pulmonary diseases, such as asthma, cystic fibrosis or chronic obstructive pulmonary disease. Thanks to recent development of culture-free high-throughput sequencing methods, the metagenomic approaches are now appropriate to detect, identify and even quantify prokaryotic or eukaryotic microorganism communities inhabiting human respiratory tract and to access the complexity of even low-burden microbe communities that are likely to play a role in chronic pulmonary diseases. In this review, we explore how metagenomics and comparative genomics studies can alleviate fungal culture bottlenecks, improve our knowledge about fungal biology, lift the veil on cross-talks between host lung and fungal microbiota, and gain insights into the pathogenic impact of these aerially transmitted fungi that affect human beings. We reviewed metagenomic studies and comparative genomic analyses of carefully chosen microorganisms, and confirmed the usefulness of such approaches to better delineate biology and pathogenesis of aerially transmitted human fungal pathogens. Efforts to generate and efficiently analyze the enormous amount of data produced by such novel approaches have to be pursued, and will potentially provide the patients suffering from chronic pulmonary diseases with a better management. This manuscript is part of the series of works presented at the "V International Workshop: Molecular genetic approaches to the study of human pathogenic fungi" (Oaxaca, Mexico, 2012).

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