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Lungs
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Cardioespiratory physiological perturbations after acute smoke-induced lung injury and during extracorporeal membrane oxygenation support in sheep
<p><span><b>Background:</b> Numerous successful therapies developed for human medicine involve animal experimentation. Animal studies that are focused solely on translational potential, may not sufficiently document unexpected outcomes. Considerable amounts of data from such studies could be used to advance veterinary science. For example, sheep are increasingly being used as models of intensive care and therefore, data arising from such models must be published. In this study, the hypothesis is that there is little information describing physiological data from sheep models of intensive care and the author aimed to analyse such data to provide biological information that is currently not available for sheep that received extracorporeal life support (ECLS) following acute smoke-induced lung injury. </span></p> <p><span><b>Methods:</b> Nineteen mechanically ventilated adult ewes undergoing intensive care during evaluation of a form of ECLS (treatment) for acute lung injury were used to collate clinical observations. Eight sheep were injured by acute smoke inhalation prior to treatment (injured/treated), while another eight were not injured but treated (uninjured/treated). Two sheep were injured but not treated (injured/untreated), while one received room air instead of smoke as the injury and was not treated (placebo/untreated). The data were then analysed for 11 physiological categories and compared between the two treated groups.</span></p> <p><span><b>Results:</b> Compared with the baseline, treatment contributed to and exacerbated the deterioration of pulmonary pathology by reducing lung compliance and the arterial oxygen partial pressure to fractional inspired oxygen (PaO<sub>2</sub>/FiO<sub>2</sub>) ratio. The oxygen extraction index changes mirrored those of the PaO<sub>2</sub>/FiO<sub>2</sub> ratio. Decreasing coronary perfusion pressure predicted the severity of cardiopulmonary injury. </span></p> <p><b>Conclusions:</b> These novel observations could help in understanding similar pathology such as that which occurs in animal victims of smoke inhalation from house or bush fires, aspiration pneumonia secondary to tick paralysis and in the management of the severe coronavirus disease 2019 (COVID-19) in humans.</p>
Tobacco smoke exposure exacerbated crystalline silica-induced lung toxicity in rats
<p>Smoking may modify the lung response to silica exposure including cancer and silicosis. Nevertheless, the precise role of exposure to tobacco smoke (TS) on the lung response to crystalline silica (CS) exposure and the underlying mechanisms need further clarification. The objectives of the present study were to determine the role of TS on lung response to CS exposure and the underlying mechanism(s). Male Fischer 344 rats were exposed by inhalation to air, CS (15 mg/m<sup>3</sup>, 6 hrs/day, 5 days), TS (80 mg/m<sup>3</sup>, 3 hrs/day, twice weekly, 6 months), or CS (15 mg/m<sup>3</sup>, 6 hrs/day, 5 days) followed by TS (80 mg/m<sup>3</sup>, 3 hrs/day, twice weekly, 6 months). The rats were euthanized 6 months and 3 weeks following initiation of the first exposure and the lung response was assessed. Silica exposure resulted in significant lung toxicity as evidenced by lung histological changes, enhanced neutrophil infiltration, increased LDH levels, enhanced oxidant production, and increased cytokine levels. The TS exposure alone had only a minimal effect on these toxicity parameters. However, the combined exposure to TS and CS exacerbated the lung response, compared to TS or CS exposure alone. Global gene expression changes in the lungs correlated with the lung toxicity severity. Bioinformatic analysis of the gene expression data demonstrated significant enrichment in functions, pathways, and networks relevant to the response to silica exposure which correlated with the lung toxicity detected. Collectively our data demonstrated an exacerbation of CS-induced lung toxicity by TS exposure and the molecular mechanisms underlying the exacerbated toxicity.</p>
Metabolic syndrome and risk of lung cancer: An analysis of Korean National Health Insurance Corporation database
<p>Introduction: Metabolic syndrome is known to increase the risk of several cancers. However, the association between lung cancer and metabolic syndrome remains unclear. Thus, we investigated the impact of metabolic syndrome on the incidence of lung cancer.</p> <p>Methods: This study enrolled participants in a health screening program provided by the Korean National Health Insurance Service between January 2009 and December 2012. The incidence of lung cancer was observed until December 2016. We analyzed the risk of lung cancer according to the presence of metabolic syndrome, metabolic syndrome components, and number of metabolic syndrome components.</p> <p>Results: During the study, 45,635 new cases of lung cancer were recorded among 9,586,753 participants. The presence of metabolic syndrome and all its components was positively associated with the risk of lung cancer in males after multivariate adjustment (hazard ratio (HR) of metabolic syndrome 1.15, 95% confidence interval (CI) = 1.12–1.18). The risk of lung cancer increased with the number of components present. The effect of metabolic syndrome on the increasing risk of lung cancer is may be higher in underweight male ever smokers than in other participants.</p> <p>Conclusion: Metabolic syndrome was associated with an increased risk of lung cancer in males. Moreover, the higher the number of metabolic syndrome components, the higher the risk of lung cancer.</p>
Full summary statistics of mixQTL for GTEx v8 Lung
The mixQTL method is described in paper doi.org/10.1101/2020.04.22.050666. Please cite the original paper if using the data.
Indirect comparison between immunotherapy alone and immunotherapy plus chemotherapy as first-line treatment for advanced non-small cell lung cancer: A systematic review
<p><b>Objectives:</b> Use of immune checkpoint inhibitors (ICIs) as first-line treatment for advanced (stage IIIB/IV) non-small cell lung cancer (NSCLC) remains controversial. Clinical trials comparing single-drug immunotherapy (IO) with immunotherapy plus chemotherapy (IC) are lacking. We aimed to compare the efficacy of IO alone with that of IC as first-line treatment for advanced NSCLC.</p> <p><b>Design: </b>Systematic review</p> <p><b>Data sources: </b>PubMed, the Cochrane Library, and Embase for related studies on NSCLC; ClinicalTrials.gov, American Society of Clinical Oncology Meeting Library, and World Conference on Lung Cancer for relevant conference abstracts.</p> <p><b>Eligibility criteria: </b>Articles<b> </b>meeting the following<b> </b>criteria were selected: (1) randomized controlled trials on NSCLC treatment, (2) all individuals in the studies had not received treatment previously, and (3) research on IO monotherapy using programmed death-1/programmed death ligand-1 (PD-L1) inhibitors or IC.</p> <p><b>Data extraction and synthesis:</b> After reading the original literature, two reviewers independently extracted the relevant information. The primary outcomes were progression-free survival (PFS), overall survival (OS), and objective response rate (ORR). We also extracted data on treatment-related adverse events and immune-related adverse events (irAEs).</p> <p><b>Results:</b> Overall, 10 randomized controlled clinical trials (n = 5765) were included. As first-line treatment for advanced NSCLC, IC tended to yield better PFS, OS, and ORR than did IO. Furthermore, IC yielded significantly better PFS than IO when tumor PD-L1 expression was at least 50% (HR: 1.81, 95% CI: 1.18–2.78) and yielded a better OS and PFS when tumor PD-L1 expression was at least 1%; IO resulted in fewer adverse events than did IC. However, the incidence of irAEs was higher for IO than for IC.</p> <p><b>Conclusions:</b> The findings of the indirect comparison indicate that IC as first-line treatment for advanced NSCLC is significantly more effective than IO in patients with PD-L1 expression in at least 50% of tumor cells.</p>
The spatial landscape of lung pathology during COVID-19 progression - processed IMC data
<p>Recent studies have provided insights into the pathology and immune response to coronavirus disease 2019 (COVID-19). However thorough interrogation of the interplay between infected cells and the immune system at sites of infection is lacking. We use high parameter imaging mass cytometry9 targeting the expression of 36 proteins, to investigate at single cell resolution, the cellular composition and spatial architecture of human acute lung injury including SARS-CoV-2. This spatially resolved, single-cell data unravels the disordered structure of the infected and injured lung alongside the distribution of extensive immune infiltration. Neutrophil and macrophage infiltration are hallmarks of bacterial pneumonia and COVID-19, respectively. We provide evidence that SARS-CoV-2 infects predominantly alveolar epithelial cells and induces a localized hyper-inflammatory cell state associated with lung damage. By leveraging the temporal range of COVID-19 severe fatal disease in relation to the time of symptom onset, we observe increased macrophage extravasation, mesenchymal cells, and fibroblasts abundance concomitant with increased proximity between these cell types as the disease progresses, possibly as an attempt to repair the damaged lung tissue. This spatially resolved single-cell data allowed us to develop a biologically interpretable landscape of lung pathology from a structural, immunological and clinical standpoint. This spatial single-cell landscape enabled the pathophysiological characterization of the human lung from its macroscopic presentation to the single-cell, providing an important basis for the understanding of COVID-19, and lung pathology in general.</p>
Crosstalk between Mast Cells and Lung Fibroblasts Is Modified by Alveolar Extracellular Matrix and Influences Epithelial Migration
<p>Datasets for the data generated and presented in the article: https://doi.org/10.3390/ijms22020506</p>
Data from: Exogenous restoration of TUSC2 expression induces responsiveness to erlotinib in wildtype epidermal growth factor receptor (EGFR) lung cancer cells through context specific pathways resulting in enhanced therapeutic efficacy
Expression of the tumor suppressor gene TUSC2 is reduced or absent in most lung cancers and is associated with worse overall survival. In this study, we restored TUSC2 gene expression in several wild type EGFR non-small cell lung cancer (NSCLC) cell lines resistant to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib and analyzed their sensitivity to erlotinib in vitro and in vivo. A significant inhibition of cell growth and colony formation was observed with TUSC2 transient and stable expression. TUSC2-erlotinib cooperativity in vitro could be reproduced in vivo in subcutaneous tumor growth and lung metastasis formation lung cancer xenograft mouse models. Combination treatment with intravenous TUSC2 nanovesicles and erlotinib synergistically inhibited tumor growth and metastasis, and increased apoptotic activity. High-throughput qRT-PCR array analysis enabling multi-parallel expression profile analysis of eighty six receptor and non-receptor tyrosine kinase genes revealed a significant decrease of FGFR2 expression level, suggesting a potential role of FGFR2 in TUSC2-enhanced sensitivity to erlotinib. Western blots showed inhibition of FGFR2 by TUSC2 transient transfection, and marked increase of PARP, an apoptotic marker, cleavage level after TUSC2-erlotinb combined treatment. Suppression of FGFR2 by AZD4547 or gene knockdown enhanced sensitivity to erlotinib in some but not all tested cell lines. TUSC2 inhibits mTOR activation and the latter cell lines were responsive to the mTOR inhibitor rapamycin combined with erlotinib. These results suggest that TUSC2 restoration in wild type EGFR NSCLC may overcome erlotinib resistance, and identify FGFR2 and mTOR as critical regulators of this activity in varying cellular contexts. The therapeutic activity of TUSC2 could extend the use of erlotinib to lung cancer patients with wildtype EGFR.
Data from: How do organisational characteristics influence teamwork and service delivery in lung cancer diagnostic assessment programmes? A mixed-methods study
Objectives: Diagnostic assessment programs (DAPs) can reduce wait times for cancer diagnosis but optimal DAP design is unknown. This study explored how organizational characteristics influenced multidisciplinary teamwork and diagnostic service delivery in lung cancer DAPs. Design: A mixed methods approach integrated data from descriptive qualitative interviews and medical record abstraction at four lung cancer DAPs. Findings were analyzed with the Integrated Team Effectiveness Model. Setting: Four DAPs at two teaching and two community hospitals in Canada Participants: Twenty-two staff were interviewed about organizational characteristics, target service benchmarks, and teamwork processes, determinants and outcomes; 314 medical records were reviewed for actual service benchmarks. Results: Formal, informal and asynchronous team processes enabled service delivery and yielded many perceived benefits at the patient, staff and service levels. However, several DAP characteristics challenged teamwork and service delivery: referral volume/workload, time since launch, days per week of operation, rural-remote population, number and type of full-time/part-time human resources, staff co-location, information systems. As a result, all sites failed to meet target benchmarks (from referral to consultation median 4.0 visits, median wait time 35.0 days). Recommendations included improved information systems, more staff in all specialties, staff co-location and expanded roles for patient navigators. Findings were captured in a conceptual framework of lung cancer DAP teamwork determinants and outcomes. Conclusions: This study identified several DAP characteristics that could be improved to facilitate teamwork and enhance service delivery, thereby contributing to knowledge of organizational determinants of teamwork and associated outcomes. Findings can be used to update existing DAP guidelines, and by managers to plan or evaluate lung cancer DAPs. Ongoing research is needed to identify ideal roles for navigators, and staffing models tailored to case volumes.
Data from: Mandible allometry in extant and fossil Balaenopteridae (Cetacea: Mammalia): the largest vertebrate skeletal element and its role in rorqual lunge-feeding
Rorqual whales (crown Balaenopteridae) are unique among aquatic vertebrates in their ability to lunge-feed. During a single lunge, rorquals rapidly engulf a large volume of prey-laden water at high speed, which they then filter to capture suspended prey. Engulfment biomechanics are mostly governed by the coordinated opening and closing of the mandibles at large gape angles, which differentially exposes the floor of the oral cavity to oncoming flow. Mouth area in rorquals is delimited by unfused bony mandibles that form kinetic linkages to each other and with the skull. The relative scale and morphology of these skeletal elements have profound consequences for the energetic efficiency of foraging in these gigantic predators. Here we performed a morphometric study of rorqual mandibles using a dataset derived from a survey of museum specimens. Across adult specimens of extant balaenopterids, mandibles range in size from ~1-6 m in length, and at their upper limit they represent the single largest osteological element of any vertebrate, living or extinct. Our analyses determined that rorqual mandibles exhibit positive allometry, whereby the relative size of these mandibles becomes greater with increasing body size. These robust scaling relationships allowed us to predict mandible length for fragmentary remains (e.g., incomplete and/or fossil specimens), as we demonstrated for two partial mandibles from the latest Miocene of California, U.S.A., and for mandibles from previously described fossil balaenopterids. Furthermore, we showed the allometry of mandible length to body size in extant mysticetes, which hints at fundamental developmental constraints in mysticetes despite their ecomorphologic differences in the feeding styles. Lastly, we outlined how our findings can be used to test hypotheses about the antiquity and evolution of lunge-feeding.
Data from: Rapid diversification of Pseudomonas aeruginosa in cystic fibrosis lung-like conditions
Chronic infection of the cystic fibrosis (CF) airway by the opportunistic pathogen Pseudomonas aeruginosa is the leading cause of morbidity and mortality for adult CF patients. Prolonged infections are accompanied by adaptation of P. aeruginosa to the unique conditions of the CF lung environment, as well as marked diversification of the pathogen into phenotypically and genetically distinct strains that can coexist for years within a patient. Little is known, however, about the causes of this diversification and its impact on patient health. Here, we show experimentally that, consistent with ecological theory of diversification, the nutritional conditions of the CF airway can cause rapid and extensive diversification of P. aeruginosa. Mucin, the substance responsible for the increased viscosity associated with the thick mucus layer in the CF airway, had little impact on within-population diversification but did promote divergence among populations. Furthermore, in vitro evolution recapitulated traits thought to be hallmarks of chronic infection, including reduced motility and increased biofilm formation, and the range of phenotypes observed in a collection of clinical isolates. Our results suggest that nutritional complexity and reduced dispersal can drive evolutionary diversification of P. aeruginosa independent of other features of the CF lung such as an active immune system or the presence of competing microbial species. We suggest that diversification, by generating extensive phenotypic and genetic variation on which selection can act, may be a key first step in the development of chronic infections.
Data from: Efficacy and safety of bevacizumab plus erlotinib versus bevacizumab or erlotinib alone in the treatment of non-small-cell lung cancer: a systematic review and meta-analysis
Objectives: Bevacizumab and erlotinib inhibit different tumour growth pathways, and both exhibit beneficial effects in the treatment of non-small-cell lung cancer (NSCLC). However, the efficacy of bevacizumab in combination with erlotinib remains controversial. Therefore, we conducted a meta-analysis to compare combination treatment with bevacizumab and erlotinib to bevacizumab or erlotinib monotherapy in the treatment of NSCLC. Methods: Randomised controlled trials (RCTs) published in PubMed, Web of Science and EMBASE were systematically reviewed. The main outcome measures included overall survival (OS), progression-free survival (PFS), overall response rate (ORR) and adverse events. Results were expressed as HRs or risk ratios (RRs) with 95% CIs. Results: 5 RCTs involving a total of 1736 patients were included in this meta-analysis. The combination of bevacizumab and erlotinib significantly improved PFS (HR=0.63, 95% CI 0.53 to 0.75; p=0.000) and the ORR (RR=1.91, 95% CI 1.19 to 3.06; p=0.007) in the second-line treatment of NSCLC compared with bevacizumab or erlotinib alone. However, no significant difference in OS was observed between the combination and monotherapy groups (HR=0.96, 95% CI 0.83 to 1.11; p=0.573). A subgroup analysis has shown that the greatest PFS benefit was associated with an age of <65 years(HR=0.74, 95% CI 0.57 to 0.96; p=0.026), Asian/Pacific Islander ethnicity (HR=0.23, 95% CI 0.10 to 0.54; p=0.001), Eastern Cooperative Oncology Group performance status (ECOG PS) 1 (HR=0.82, 95% CI 0.68 to 0.98; p=0.033), stage IIIB or IV disease (HR=0.68, 95% CI 0.57 to 0.82; p=0.000) and no history of smoking (HR=0.48, 95% CI 0.32 to 0.71; p=0.000). The incidence of grade 3/4 adverse events such as rash and diarrhoea was higher in the combination group than in the monotherapy group. Conclusions: The addition of bevacizumab to erlotinib can significantly improve PFS and the ORR in the second-line treatment of NSCLC with an acceptable and manageable risk of rash and diarrhoea. Further well-conducted, large-scale trials are needed to validate these findings.
Data from: Cytoskeleton structure and total methylation of mouse cardiac and lung tissue during space flight
The purpose of this work was to evaluate the protein and mRNA expression levels of multiple cytoskeletal proteins in the cardiac and lung tissue of mice that were euthanized onboard the United States Orbital Segment of the International Space Station 37 days after the start of the SpaceX-4 mission (September 2014, USA). The results showed no changes in the cytoskeletal protein content in the cardiac and lung tissue of the mice, but there were significant changes in the mRNA expression levels of the associated genes, which may be due to an increase in total genome methylation. The mRNA expression levels of DNA methylases, the cytosine demethylases Tet1 and Tet3, histone acetylase and histone deacetylase did not change, and the mRNA expression level of cytosine demethylase Tet2 was significantly decreased.
Data from: Changes in the bacterial microbiota in gut, blood, and lungs following acute LPS instillation into mice lungs
Introduction: Previous reports have shown that the gastrointestinal (GI) bacterial microbiota can have profound effects on the lungs, which has been described as the "gut-lung axis". However, whether a "lung-gut" axis exists wherein acute lung inflammation perturbs the gut and blood microbiota is unknown. Methods: Adult C57/Bl6 mice were exposed to one dose of LPS or PBS instillation (n = 3 for each group) directly into lungs. Bacterial microbiota of the bronchoalveolar lavage fluid, blood, and cecum were determined using 454 pyrotag sequencing and quantitative polymerase chain reaction (qPCR) at 4 through 168 hours post-instillation. We then investigated the effects of oral neomycin and streptomycin (n = 8) on the microbiota at 4 and 24 hours post LPS instillation versus control treatment (n = 5 at baseline and 4 hours, n = 7 at 24 hours). Results: At 24 hours post LPS instillation, the total bacterial count was significantly increased in the cecum (P<0.05); whereas the total bacterial count in blood was increased at 4, 48, and 72 hours (P<0.05). Antibiotic treatment reduced the total bacteria in blood but not in the cecum. The increase in total bacteria in the blood correlated with Phyllobacteriaceae OTU 40 and was significantly reduced in the blood for both antibiotic groups (P<0.05). Conclusion: LPS instillation in lungs leads to acute changes in the bacterial microbiota in the blood and cecum, which can be modulated with antibiotics.
Data from: The host response to the lung microbiome in Chromic Obstructive Pulmonary Disease
Rationale: The relatively sparse but diverse microbiome in human lungs may become less diverse in chronic obstructive pulmonary disease (COPD). This article examines the relationship of this microbiome to emphysematous tissue destruction, number of terminal bronchioles, infiltrating inflammatory cells, and host gene expression. Methods: Culture-independent pyrosequencing microbiome analysis was used to examine the V3–V5 regions of bacterial 16S ribosomal DNA in 40 samples of lung from 5 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage 4) and 28 samples from 4 donors (controls). A second protocol based on the V1–V3 regions was used to verify the bacterial microbiome results. Within lung tissue samples the microbiome was compared with results of micro–computed tomography, infiltrating inflammatory cells measured by quantitative histology, and host gene expression. Measurements and Main Results: Ten operational taxonomic units (OTUs) was found sufficient to discriminate between control and GOLD stage 4 lung tissue, which included known pathogens such as Haemophilus influenzae. We also observed a decline in microbial diversity that was associated with emphysematous destruction, remodeling of the bronchiolar and alveolar tissue, and the infiltration of the tissue by CD4+ T cells. Specific OTUs were also associated with neutrophils, eosinophils, and B-cell infiltration (P < 0.05). The expression profiles of 859 genes and 235 genes were associated with either enrichment or reductions of Firmicutes and Proteobacteria, respectively, at a false discovery rate cutoff of less than 0.1. Conclusions: These results support the hypothesis that there is a host immune response to microorganisms within the lung microbiome that appears to contribute to the pathogenesis of COPD.
MORPHOLOGICAL ASPECTS OF FEATURES OF CHRONIC LUNG IRRADIATION IN EXPERIMENTAL,
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STRUCTURAL CHANGES IN THE BRONCHUS AND LUNGS OF YOUNG CHILDREN WITH BRONCHOPULMONARY DYSPLASIA
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Pathological images of non-small cell lung cancer
<p>The dataset comprises lung cancer patient information and pathology images utilized for the analysis of our study. These are anonymized data from cases in our cohort for which patient consent was obtained for public deposition. </p> <p>Patient information for original cohort and validation cohort is described in the Excle files, "original_cohort_patient_info.xlsx" and "validation_cohort_patient_info.xlsx", respectively. </p> <p>These Excel files contain information on sex, age, smoking history, pathological stage, histology, lymphovascular invasion, pleural invasion, lymph node metastasis, adjuvant treatment, survival outcomes and file names for pathological images of each patient. Each patient has two files of Whole Slide Images files (format: .npdi) including hematoxylin & eosin staining ("XXX_h.ndpi") and immunohistochemistry stainig for PD-L1 ("XXX_p.ndpi").</p>
Integration of Single-Cell Analysis and Mendelian Randomization Reveals NET1 as a Potential Key Player in Lung Cancer Pathogenesis
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