Small Airways Research Articles

Impact of altitude on the dosage of indoor particulates entering an individual’s small airways

The complexity of indoor particulate exposure intensifies at higher altitudes owing to the increased lung capacity that residents develop to meet the higher oxygen demands. Altitude variations impact atmospheric pressure and alter particulate dynamics in ambient air and the human respiratory tract, complicating particulate inhalation. This study assessed the fraction of PM2.5 and PM10 entering small airways. This assessment covered an altitude range from 400 m above sea level to 3650 m, and an in vitro respiratory tract model was used. The experimental results confirmed that with increasing altitude, the penetration fractions of PM2.5 and PM10 significantly increased from 0.133 ± 0.031 and 0.141 ± 0.045 to 0.404 ± 0.159 and 0.353 ± 0.132, respectively. Additionally, the computational fluid dynamics simulation results revealed that among particles with sizes of 0.1 to 10 µm, the 7.5-μm particles exhibited the most substantial reduction in deposition in the upper airway, displaying a decrease of 6.27%. Our findings underscore the health risks faced by low-altitude residents during acclimatization to higher altitudes, as they experience heightened exposure to particulate matter sources.

Combined effect of changes in NO2, O3, PM2.5, SO2 and CO concentrations on small airway dysfunction.

When multiple complex air pollutants are combined in real-world settings, the reliability of estimating the effect of a single pollutant is questionable. This study aimed to investigate the combined effects of changes in air pollutants on small airway dysfunction (SAD). We analysed Korea National Health and Nutrition Examination Survey (KNHANES) V-VIII database from 2010 to 2018 to elucidate the associations between annual changes in air pollutants over a previous 5-year period and small airway function. We estimated the annual concentrations of five air pollutants: NO2, O3, PM2.5, SO2 and CO. Forced expiratory flow between 25% and 75% of vital capacity (FEF25%-75%) <65% was defined as SAD. Using the quantile generalized-Computation (g-Computation) model, the combined effect of the annual changes in different air pollutants was estimated. A total of 29,115 individuals were included. We found significant associations between SAD and the quartiles of annual changes in NO2 (OR = 1.10, 95% CI = 1.08-1.12), O3 (OR = 1.03, 95% CI = 1.00-1.05), PM2.5 (OR = 1.03, 95% CI = 1.00-1.05), SO2 (OR = 1.04, 95% CI = 1.02-1.08) and CO (OR = 1.16, 95% CI = 1.12-1.19). The combined effect of the air pollutant changes was significantly associated with SAD independent of smoking (OR = 1.31, 95% CI = 1.26-1.35, p-value <0.001), and this trend was consistently observed across the entire study population and various subgroup populations. As the estimated risk of SAD, determined by individual-specific combined effect models, increased and the log odds for SAD increased linearly. The combined effect of annual changes in multiple air pollutant concentrations were associated with an increased risk of SAD.

Subclinical pleuro-pulmonary disease in patients with SLE: functional and radiological methods

Abstract Background Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with highest prevalence of chest involvement; however, early detection of subclinical pleuropulmonary diseases may improve the quality of life and prognosis of patients. This study aimed to identify the subclinical pleuro-pulmonary involvement in SLE patients without respiratory symptoms. Methods A total of 228 patients diagnosed with SLE were recruited and subjected to high-resolution computed tomography (HRCT) chest, ultrasound (US) chest, and spirometry for further evaluation and finding of sub-clinical signs. Results Around 52.63% of patients had pulmonary involvement in HRCT, while in US, it was 73.68%. Ground glass opacity was observed in 31.58% of HRCT cases, and &gt; 1/3 of patients had pleural thickness in US. Spirometry showed that 26.32% of patients had small airway disease. SLE patients with subclinical lung involvement were significantly female and younger and had shorter disease duration, p &lt; 0.05 for all. SLE severity showed a significant negative correlation with lung function, and was positively correlated with pleural thickness and effusion, and pleural nodules in US finding. However, diaphragmatic excursion showed a negative correlation. Moreover, ground glass opacities, honey combing opacities, interlobular septal thickening, pleural thickness, and effusion in HRCT showed positive correlation with disease severity, p &lt; 0.001 for all, yet, the mosaic pattern showed a negative relationship. Conclusion The radiological assessments of SLE patients via HRCT and ultrasound unveiled prevalent findings such as ground glass opacities and pleural abnormalities. The severity of SLE correlated significantly with pulmonary function tests in a negative way, plus the positive correlation with lung opacities and pleural abnormalities.

A pilot study to assess the effects of preventing fluid retention in the legs by wearing compression stockings on overnight airway narrowing in mild asthma.

Nocturnal asthma is a sign of asthma worsening and could be partially due to more fluid drawn into the thorax during sleep by gravitational force and/or pharyngeal collapse in those with obstructive sleep apnea. Wearing compression stockings during the day reduces fluid shift from the legs to the neck overnight. However, the potential effect of wearing compression stockings to reduce fluid accumulation in the leg and to improve nocturnal small airway narrowing in patients with asthma has not been investigated. This study investigates whether reducing leg fluid volume by wearing compression stockings during the day would attenuate small airway narrowing in patients with asthma before and after sleep. We enrolled 11 participants with asthma. All participants underwent overnight polysomnography with or without wearing compression stockings for 2weeks. Before and after sleep, leg fluid volume (LFV) was measured by bioelectrical impedance, and airway narrowing was primarily assessed by respiratory system resistance and reactance at 5Hz (R5 and X5 respectively) using oscillometry. After 2weeks of wearing compression stockings, the LFV measured in the evening was reduced (∆ = - 192.6 ± 248.3ml, p = 0.02), and R5 and X5 improved (∆ = - 0.7 ± 0.9 cmH2O/L/s, p = 0.03 and 0.2 ± 1.4 cmH2O/L/s, p = 0.05 respectively). No changes were observed in the morning. Preventing fluid retention in the legs by wearing compression stockings for 2weeks during the day, reduced LFV and airway narrowing in the evening in all participants with asthma, but not in the morning after sleep.

SARS-CoV-2 spike protein-ACE2 interaction increases carbohydrate sulfotransferases and reduces N-acetylgalactosamine-4-sulfatase by p38 MAPK

Immunostaining in lungs of patients who died with COVID-19 infection showed increased intensity and distribution of chondroitin sulfate and decline in N-acetylgalactostamine-4-sulfatase (Arylsulfatase B; ARSB). To explain these findings, human small airway epithelial cells were exposed to the SARS-CoV-2 spike protein receptor binding domain (SPRBD) and transcriptional mechanisms were investigated. Phospho-p38 MAPK and phospho-SMAD3 increased following exposure to the SPRBD, and their inhibition suppressed the promoter activation of the carbohydrate sulfotransferases CHST15 and CHST11, which contributed to chondroitin sulfate biosynthesis. Decline in ARSB was mediated by phospho-38 MAPK-induced N-terminal Rb phosphorylation and an associated increase in Rb-E2F1 binding and decline in E2F1 binding to the ARSB promoter. The increases in chondroitin sulfotransferases were inhibited when treated with phospho-p38-MAPK inhibitors, SMAD3 (SIS3) inhibitors, as well as antihistamine desloratadine and antibiotic monensin. In the mouse model of carrageenan-induced systemic inflammation, increases in phospho-p38 MAPK and expression of CHST15 and CHST11 and declines in DNA-E2F binding and ARSB expression occurred in the lung, similar to the observed effects in this SPRBD model of COVID-19 infection. Since accumulation of chondroitin sulfates is associated with fibrotic lung conditions and diffuse alveolar damage, increased attention to p38-MAPK inhibition may be beneficial in ameliorating Covid-19 infections.

Improving asthma outcomes: Clinicians’ perspectives on peripheral airways

Disease of the peripheral (or small) airways is fundamental in asthma, being closely related to symptoms (or lack of control them), airway hyperresponsiveness, spirometric abnormalities, risk of loss of control or exacerbations and inflammation. Current technology now allows routine measurement of peripheral airway function. Having a working concept of peripheral airways disease in asthma is arguably, very useful to clinicians and beneficial to patients because it allows a more comprehensive assessment of asthma severity (rather than just symptoms alone which is the norm), tracking of progress or deterioration and assessing response to treatment. Oscillometry is a sensitive way to monitor the peripheral airways, while multiple breath nitrogen washout parameters are excellent measures of future risk. In the longer term, physiologic measurements will be crucial in research to define causes and find new, disease modifying treatments.

Improved small airway dysfunction in severe asthma with clinical remission by anti-interleukin-5/interleukin-5 receptor α

Improved small airway dysfunction in severe asthma with clinical remission by anti-interleukin-5/interleukin-5 receptor α

Dysfunctional neutrophil type 1 interferon responses in preschool children with recurrent wheezing and IL-4–mediated aeroallergen sensitization

BackgroundThe innate mechanisms associated with viral exacerbations in preschool children with recurrent wheezing are not understood. ObjectiveWe assessed differential gene expression in blood neutrophils from preschool children with recurrent wheezing, stratified by aeroallergen sensitization, at baseline and after exposure to polyinosinic-polycytidylic acid (poly(I:C)). We also examined whether poly(I:C)-stimulated blood neutrophils influenced airway epithelial gene expression. MethodsBlood neutrophils were purified and cultured overnight with poly(I:C) and underwent next-generation sequencing with Reactome pathway analysis. Primary human small airway epithelial cells were treated with poly(I:C)-treated neutrophil culture supernatants and were analyzed for Type 1 interferon gene expression with a targeted array. Symptoms and exacerbations were assessed in participants over 12 months. Results436 genes were differently expressed in neutrophils from children with versus without aeroallergen sensitization at baseline, with significant downregulation of Type 1 interferons. These Type 1 interferons were significantly upregulated in sensitized children after poly(I:C) stimulation. Confirmatory experiments demonstrated similar upregulation of Type 1 interferons in IL-4 treated neutrophils stimulated with poly(I:C). Poly(I:C)-treated neutrophil supernatants from children with aeroallergen sensitization also induced a Type 1 interferon response in epithelial cells. Children with aeroallergen sensitization also had higher symptom scores during exacerbations and these symptom differences persisted for three days after prednisolone treatment. ConclusionsType 1 interferon responses are dysregulated in preschool children with aeroallergen sensitization, which is in turn associated with exacerbation severity. Given the importance of Type 1 interferon signaling in viral resolution, additional studies of neutrophil Type 1 interferon responses are needed in this population.

Phenotyping of COPD with MRI in comparison to same-day CT in a multi-centre trial

ObjectivesA prospective, multi-centre study to evaluate concordance of morphologic lung MRI and CT in chronic obstructive pulmonary disease (COPD) phenotyping for airway disease and emphysema.MethodsA total of 601 participants with COPD from 15 sites underwent same-day morpho-functional chest MRI and paired inspiratory-expiratory CT. Two readers systematically scored bronchial wall thickening, bronchiectasis, centrilobular nodules, air trapping and lung parenchyma defects in each lung lobe and determined COPD phenotype. A third reader acted as adjudicator to establish consensus. Inter-modality and inter-reader agreement were assessed using Cohen’s kappa (im-κ and ir-κ).ResultsThe mean combined MRI score for bronchiectasis/bronchial wall thickening was 4.5/12 (CT scores, 2.2/12 for bronchiectasis and 6/12 for bronchial wall thickening; im-κ, 0.04–0.3). Expiratory right/left bronchial collapse was observed in 51 and 47/583 on MRI (62 and 57/599 on CT; im-κ, 0.49–0.52). Markers of small airways disease on MRI were 0.15/12 for centrilobular nodules (CT, 0.34/12), 0.94/12 for air trapping (CT, 0.9/12) and 7.6/12 for perfusion deficits (CT, 0.37/12 for mosaic attenuation; im-κ, 0.1–0.41). The mean lung defect score on MRI was 1.3/12 (CT emphysema score, 5.8/24; im-κ, 0.18–0.26). Airway-/emphysema/mixed COPD phenotypes were assigned in 370, 218 and 10 of 583 cases on MRI (347, 218 and 34 of 599 cases on CT; im-κ, 0.63). For all examined features, inter-reader agreement on MRI was lower than on CT.ConclusionConcordance of MRI and CT for phenotyping of COPD in a multi-centre setting was substantial with variable inter-modality and inter-reader concordance for single diagnostic key features.Clinical relevance statementMRI of lung morphology may well serve as a radiation-free imaging modality for COPD in scientific and clinical settings, given that its potential and limitations as shown here are carefully considered.Key Points• In a multi-centre setting, MRI and CT showed substantial concordance for phenotyping of COPD (airway-/emphysema-/mixed-type).• Individual features of COPD demonstrated variable inter-modality concordance with features of pulmonary hypertension showing the highest and bronchiectasis showing the lowest concordance.• For all single features of COPD, inter-reader agreement was lower on MRI than on CT.

Large airway T cells in adults with former bronchopulmonary dysplasia

BackgroundBronchopulmonary Dysplasia (BPD) in infants born prematurely is a risk factor for chronic airway obstruction later in life. The distribution of T cell subtypes in the large airways is largely unknown.ObjectiveTo characterize cellular and T cell profiles in the large airways of young adults with a history of BPD.MethodsForty-three young adults born prematurely (preterm (n = 20), BPD (n = 23)) and 45 full-term-born (asthma (n = 23), healthy (n = 22)) underwent lung function measurements, and bronchoscopy with large airway bronchial wash (BW). T-cells subsets in BW were analyzed by immunocytochemistry.ResultsThe proportions of both lymphocytes and CD8 + T cells in BW were significantly higher in BPD (median, 6.6%, and 78.0%) when compared with asthma (3.4% and 67.8%, p = 0.002 and p = 0.040) and healthy (3.8% and 40%, p < 0.001 and p < 0.001). In all adults born prematurely (preterm and BPD), lymphocyte proportion correlated negatively with forced vital capacity (r= -0.324, p = 0.036) and CD8 + T cells correlated with forced expiratory volume in one second, FEV1 (r=-0.448, p = 0.048). Correlation-based network analysis revealed that lung function cluster and BPD-birth cluster were associated with lymphocytes and/or CD4 + and CD8 + T cells. Multivariate regression analysis showed that lymphocyte proportions and BPD severity qualified as independent factors associated with FEV1.ConclusionsThe increased cytotoxic T cells in the large airways in young adults with former BPD, suggest a similar T-cell subset pattern as in the small airways, resembling features of COPD. Our findings strengthen the hypothesis that mechanisms involving adaptive and innate immune responses are involved in the development of airway disease due to preterm birth.

Differential expression of mast cells in the small airways and alveolar septa of current smokers and patients with small airway disease and COPD.

COPD patients suffer from dysregulated and suppressed immune functionality, determined by their loss of degranulating capacity. Here we provide crucial information on the presence of degranulated mast cells (MCs) in COPD airways and demonstrate their relationship to lung physiology and airway remodelling. Small airway lung resections from non-smoking controls (NC), normal lung function smokers (NLFS), small airway disease (SAD), and mild-to-moderate COPD current smokers (COPD-CS) and ex-smokers (COPD-ES) were dual immuno-stained with MC tryptase and degranulation marker lysosome-associated membrane protein (LAMP)-1. Total MCs, degranulating MCs and non-MCs were enumerated in small airway epithelium and subepithelium, and in alveolar septa. In the small airway wall subepithelial areas, COPD-CS and COPD-ES patients had significantly lower MCs than the NC group (p<0.05), although the numbers were considerably higher in the small airway epithelium (p<0.01). Degranulating non-MCs were higher in SAD (p<0.05) than in COPD in the small airway subepithelium. In contrast, there were significant increases in total MCs (degranulated and non-degranulated) and degranulated non-MCs in the alveolar septum of COPD patients compared with the NC group (p<001). The lower numbers of MCs in the subepithelium correlated with lower forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) and forced expiratory flow at 25-75% of FVC (FEF25-75%), higher smoking rates in COPD patients, and increased small airway wall thickness and extracellular matrix. The increase in MCs in the alveolar septum negatively correlated with FEF25-75%. This study is the first to assess the differential pattern of MC, degranulating MC and non-MC populations in the small airways and alveoli of COPD patients. The spatial positioning of the MCs within the airways showed variable correlations with lung function.

HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing

BackgroundSmall airway remodelling is a vital characteristic of chronic obstructive pulmonary disease (COPD), which is mainly caused by epithelial barrier dysfunction and epithelial-mesenchymal transition (EMT). Recent studies have indicated that histone deacetylase 6 (HDAC6) plays an important role in the dysregulation of epithelial function. In this study, we investigated the therapeutic effects and underlying mechanisms of an inhibitor with high selectivity for HDAC6 in COPD.MethodsCigarette smoke (CS) exposure was used to establish a CS-induced COPD mouse model. CAY10603 at doses of 2.5 and 10 mg/kg was injected intraperitoneally on alternate days. The protective effects of CAY10603 against CS-induced emphysema, epithelial barrier function and small airway remodeling were evaluated using hematoxylin and eosin (H&E) staining, Masson’s trichrome staining, immunohistochemical staining, and western blot. The human lung bronchial epithelial cell line (HBE) was used to elucidate the underlying molecular mechanism of action of CAY10603.ResultsHDAC6 levels in the lung homogenates of CS-exposed mice were higher than that those in control mice. Compared to the CS group, the mean linear intercept (MLI) of the CAY10603 treatment group decreased and the mean alveolar number (MAN)increased. Collagen deposition was reduced in groups treated with CAY10603. The expression of α-SMA was markedly upregulated in the CS group, which was reversed by CAY10603 treatment. Conversely, E-cadherin expression in the CS group was further downregulated, which was reversed by CAY10603 treatment. CAY10603 affects the tight junction protein expression of ZO-1 and occludin. ZO-1 and occludin expression were markedly downregulated in the CS group. After CAY10603treatment, the protein expression level of ZO-1 and occludin increased significantly. In HBE cells, Cigarette smoke extract (CSE) increased HDAC6 levels. CAY10603 significantly attenuated the release of TGF-β1 induced by CSE. CAY10603 significantly increased the E-cadherin levels in TGF-β1 treated HBE cells, while concurrently attenuated α-SMA expression. This effect was achieved through the suppression of Smad2 and Smad3 phosphorylation. CAY10603 also inhibited TGF-β1 induced cell migration.ConclusionsThese findings suggested that CAY10603 inhibited CS induced small airway remodelling by regulating epithelial barrier dysfunction and reversing EMT via the TGF-β1/Smad2/3 signalling pathway.

MicroRNA-377-3p exacerbates chronic obstructive pulmonary disease through suppressing ZFP36L1 expression and inducing lung fibroblast senescence

Chronic obstructive pulmonary disease (COPD) is a leading aging related cause of global mortality. Small airway narrowing is recognized as an early and significant factor for COPD development. Senescent fibroblasts were observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition and senescence-associated secretory phenotype (SASP). On the basis of our previous study, we further investigated the the causes for the increased levels of miR-377-3p in the blood of COPD patients, as well as its regulatory function in the pathological progression of COPD. We found that the majority of up-regulated miR-377-3p was localized in lung fibroblasts. Inhibition of miR-377-3p improved chronic smoking-induced COPD in mice. Mechanistically, miR-377-3p promoted senescence of lung fibroblasts, while knockdown of miR-377-3p attenuated bleomycin-induced senescence in lung fibroblasts. We also identified ZFP36L1 as a direct target for miR-377-3p that likely mediated its pro senescence activity in lung fibroblasts. Our data reveal that miR-377-3p is crucial for COPD pathogenesis, and may serve as a potential target for COPD therapy.

A modern approach to surgical tactics in patients with residual post-tuberculosis changes of lungs

In patients with residual changes after the treatment of destructive forms of tuberculosis (TB), the risk of recurrence of the disease increases significantly. The study of the surgical material of patients with pulmonary TB as a result of the progression of residual post-tuberculosis changes a year or more after the completion of anti-tuberculosis therapy makes it possible to justify the need for surgery in this category of patients. Objective. To substantiate surgical tactics in patients with residual post-tuberculosis lung changes. Materials and methods. The analysis of 1121 adult patients who underwent surgery from 2015 to 2021 for etiologically verified pulmonary TB and completed anti-tuberculosis therapy more than a year before the operation. Of these, 176 patients were divided into two comparable groups: the main group included 37 patients in whom non-tuberculosis mycobacteria (NTMB) DNA was found in the surgical material, the comparison group included 139 patients in whom NTMB was not found in the surgical material. All patients underwent a comprehensive microbiological and morphological examination of the surgical material. Results. In the comparison group, in the majority of operated patients with microbiological screening of surgical material, the etiological diagnosis was positive: the most informative method for both destructive forms of pulmonary TB and forms without destruction was the real-time PCR method: in 82.0% and 87.2% of positive results, respectively, and luminescent microscopy, which allowed to identify acid-resistant Mycobacteria in 67.2% of cases with destructive forms of TB and in 73.1% – without lung destruction In the comparison group, in 19 (13.2%) patients, no evidence of TB was obtained by any screening method, but morphologic examination of surgical material showed the presence of TB inflammation with high activity in 11 (58.0%) and moderate activity in 8 (42.0%) patients. In the main group species identification of NTMB in the surgical material was obtained in the majority of cases, both in forms without destruction of lung tissue and in destructive forms – in 72.2 and 63.3% of patients, respectively, slow-growing NTMB prevailing. Fast-growing NTMB were detected in isolated cases. Morphological examination of the surgical material in a group of patients with NTMB revealed structural changes in the lungs that affected the air parenchyma and/or small airways in areas of the lungs free from TB foci, which should be taken into account when planning surgical intervention. Conclusion. Surgical treatment immediately after completion of the course of anti-tuberculosis therapy in case of formation of residual post-tuberculosis changes is the method of choice in the complex treatment of this category of patients.

The Impact of Heat-Not-Burn, E-Cigarettes, and Cigarettes on Small Airway Function.

E-cigarettes and heated tobacco products (HTPs) are gaining worldwide significance. The tobacco industry is promoting these products as healthier alternatives to conventional cigarettes. In this four-arm crossover study, we examined the acute effects of cigarette smoking, vaping IQOS, or vaping e-cigarettes (with or without nicotine) on hemodynamics, arterial stiffness, and small airways. Twenty subjects (10 male, 10 female), all occasional smokers, completed each study arm. There was at least a 48h washout period before each test day. Arterial stiffness and peripheral and central hemodynamics were assessed using Mobil-O-Graph™ (I.E.M., Germany), whereas tremoFlo® c-100 (Thoracic Medical Systems Inc) was used to evaluate the effects on the small airways and resistance. Cigarettes, IQOS, e-cigarettes containing nicotine, and nicotine-free e-cigarettes had similar effects on peripheral and central hemodynamics as well as on arterial stiffness. We observed a significant increase in all parameters. However, only nicotine-containing products lead to increased bronchial obstruction, higher reactance, and a higher tidal volume. Therefore, we concluded that cigarettes, IQOS, and e-cigarettes have similar effects on hemodynamics. No differences were observed between the nicotine-containing and nicotine-free e-cigarettes. All nicotine-containing products also influence small airways. These findings suggest that e-cigarettes and HTPs are not healthier alternatives than conventional cigarettes.

Circadian rhythm and variability of large and small airway spirometric variables in healthy individuals.

To assess the diurnal rhythm and variability of lung function in healthy individuals, encompassing both large and small airways. A prospective study enrolled 35 healthy adults without a history of smoking. Initial spirometry and a bronchodilation test were performed using the Jaeger spirometer, followed by a seven-day continuous home monitoring using the GOSPT2000. We evaluated repeatability using the intraclass correlation coefficient and agreement through linear regression and Bland-Altman analyses. Circadian rhythm and variability in spirometric measurements were analyzed using the coefficient of variation (CV) and daily variation rate. The GOSPT2000 demonstrated strong repeatability and high agreement with the Jaeger spirometer. Notable findings included a decrease in nocturnal forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and FEV3 by 44, 59, and 53 mL, respectively. In contrast, peak expiratory flow at noon showed an increase of 0.143L/min. Small-airway variables, including forced expiratory flow at 50% and 75% of the FVC and maximum midexpiratory flow, showed no significant diurnal variation. The nocturnal CV for large-airway variables was ≤ 4%, while for small-airway variables, it was ≤ 11.89%. This study has established a spectrum of variability for both large and small airways in healthy populations. The variability of small-airway variables is higher than that of large-airway variables. The investigation into the diurnal rhythms and variability characteristics of both large and small airway variables in the healthy population can serve as a foundation for diagnosing asthma or assessing the efficacy of asthma treatments.

ПОСТТУБЕРКУЛЕЗНАЯ ОБСТРУКТИВНАЯ БОЛЕЗНЬ ЛЕГКИХ (обзор зарубежной литературы)

Abstract. Introduction. Post-tuberculous obstructive pulmonary disease has been considered as a chronic disease for the last decade. Despite successful clinical cure of tuberculosis, up to 50% of patients have post-tuberculous obstructive pulmonary disease, defined as the “signs of chronic respiratory distress, with or without symptoms, at least partially attributable to prior pulmonary tuberculosis”. Aim. To consider the epidemiological and pathophysiological relationships between chronic airway obstruction in COPD and tuberculosis and to highlight the diagnostic and therapeutic approaches to managing patients with post-tuberculous obstructive pulmonary disease. Materials and Methods. We searched available information databases up to June 2023 using key terms, i.e. COPD, tuberculosis associated with COPD, post-tuberculous obstructive pulmonary disease. Results and Discussion. Post-tuberculous obstructive pulmonary disease is one of the many TB complications that significantly affects the economic, social, and psychological well- being of individuals, families, and communities. Post-tuberculous obstructive pulmonary disease includes a group of heterogeneous conditions affecting the large and small airways, such as bronchiectasis or obstructive airways; lung parenchyma, pleura, and/or pulmonary vasculature, and may present with symptoms partly associated with past pulmonary tuberculosis. Post-tuberculous obstructive pulmonary disease results from a complex interaction between human immune reactivity, pathogens, and environmental factors that affects long-term respiratory health. Major risk factors for post-tuberculous obstructive pulmonary disease include smoking, low socioeconomic status, vitamin D deficiency, and diabetes mellitus. People with post-tuberculous obstructive pulmonary disease have a reduced life expectancy and an increased risk of TB recurrence. Conclusions. Currently, due to the lack of controlled clinical trials, there are no generally accepted recommendations for the diagnosis and treatment of post-tuberculous obstructive pulmonary disease. The management of patients with post-tuberculous obstructive pulmonary disease mainly includes adjuvant therapy used in other chronic obstructive pulmonary diseases and in pulmonary rehabilitation. Early diagnosis and timely treatment are essential to limit lung damage.

Small airway reversibility, TNF alpha levels and female gender are associated with cardiopulmonary exercising testing abnormalities in children with post-covid respiratory symptoms

Small airway reversibility, TNF alpha levels and female gender are associated with cardiopulmonary exercising testing abnormalities in children with post-covid respiratory symptoms

The role of small airways on persistent bronchial hyper-responsiveness (BHR) in asthma children with asthma: the comparison of predicted percentage value vs Z score of spirometry

The role of small airways on persistent bronchial hyper-responsiveness (BHR) in asthma children with asthma: the comparison of predicted percentage value vs Z score of spirometry

Research progress on the pathogenesis of chest tightness variant asthma characterized by chest tightness.

Chest tightness variant asthma (CTVA) is an atypical form of asthma with chest tightness as the sole or predominant symptom. The underlying receptors for chest tightness are bronchial C-fibers or rapidly adapting receptors. The nerve impulses are transmitted via the vagus nerve and processed in different regions of the cerebral cortex. Chest tightness is associated with sensory perception, and CTVA patients may have heightened ability to detect subtle changes in lung function, but such sensory perception is unrelated to respiratory muscle activity, lung hyperinflation, or mechanical loading of the respiratory system. Airway inflammation, pulmonary ventilation dysfunction (especially involving small airways), and airway hyperresponsiveness may underlie the sensation of chest tightness. CTVA patients are prone to comorbid anxiety and depression, which share similar central nervous system processing pathways with dyspnea, suggesting a possible neurological basis for the development of CTVA. This article examines the recognition and mechanisms of chest tightness, and explores the pathogenesis of CTVA, focusing on its association with airway inflammation, ventilation dysfunction, airway hyperresponsiveness, and psychosocial factors.