搜索结果：Advances in respiratory medicine

Respiratory seasonal viral infections remain one of the most important issues in community medicine. The heterogeneity of etiological agents and the characteristics of the hosts airway antiviral defenses account for the complex management of these infections. The clinical consequence of this picture is that, despite the widespread use of vaccination as the primary prevention strategy, the rates of acute respiratory complications remain still high. In addition, they determine post-infectious fatigue and organ dysfunction. Inflammation and oxidative stress are the principal pathogenic mechanisms responsible for clinical complications during respiratory seasonal viral infections. Nowadays, a growing body of evidence indicates that adjunctive nutritional support can contribute to relieve the symptoms during the acute and subacute phases of respiratory viral infections. We assess the data in the literature regarding the combination of L-Arginine and Liposomal Vitamin C as adjuvant treatment for respiratory seasonal viral infections. The database of the National Library of Medicine (PubMed) was searched using the keywords "L-Arginine, Vitamin C, dietary supplements, seasonal respiratory viral infections". The treatment of symptoms during acute and post-acute respiratory viral infections requires an integrated approach that includes vitamins and nutritional supplementation. The combination of L-Arginine and Liposomal Vitamin C seems to represent a nutritional support able to mitigate symptoms occurring during the acute or post-acute phase of infection.

Surfactant Protein D (SP-D) is a critical immunomodulatory collectin maintaining alveolar homeostasis. Obstructive sleep apnea (OSA)-related intermittent hypoxia (IH) disrupts pulmonary surfactant integrity; however, severity-dependent SP-D dynamics remain incompletely characterized. This study explores SP-D as a potential indicator of IH-induced alveolar stress and evaluates whether Galectin-3 (Gal-3) inhibition modulates surfactant homeostasis. Forty adult male Sprague-Dawley rats (8 per group) were randomized to Control (normoxia), Moderate IH (MIH; 15-30 events/hour), Severe IH (SIH; 30-60 events/hour), MIH + Gal-3 inhibitor (Modified Citrus Pectin, 800 mg/kg/day), or SIH + Gal-3 inhibitor. IH exposure lasted 8 h/day for 10 days. Outcomes included circulating SP-D, Surfactant Protein B (SP-B), inflammatory markers, physiological parameters, and histopathological lung injury scores assessed via American Thoracic Society guidelines. SP-D levels showed numerical reductions with increasing IH severity (Control: 1969.07 pg/mL [IQR: 262.15]; SIH: 1404.30 pg/mL [IQR: 351.88]), representing a 28.6% decrease. However, between-group variability resulted in non-significant omnibus testing (Kruskal-Wallis p = 0.187). Gal-3 inhibition elevated SP-D levels, particularly in severe IH (2133.95 pg/mL [IQR: 1240.70]), though high inter-individual variability was observed (CV = 58.1%). SP-B showed significant suppression under moderate IH (p = 0.019) with restoration by treatment. Exploratory correlation analysis revealed moderate positive associations between SP-D and heart rate (r = 0.587) and respiratory rate (r = 0.419) in severe IH, though these did not reach statistical significance (p = 0.126 and p = 0.301, respectively). Histologically, severe IH induced diffuse alveolar damage (total lung score: 19.67 &#xb1; 0.82). Gal-3 inhibition produced context-dependent effects: protective in severe IH but paradoxically exacerbating inflammation under moderate IH (29.20 &#xb1; 4.64 vs. 20.00 &#xb1; 4.34; p < 0.05). Gal-3 inhibition significantly attenuated cardiac injury (injury score: 0.00 &#xb1; 0.00 vs. 7.17 &#xb1; 0.75 in severe IH; p < 0.001, &#x3b7;2 = 0.859). SP-D demonstrates severity-associated alterations consistent with alveolar epithelial stress during IH, though high variability limits definitive biomarker validation in this sample. Gal-3 inhibition modulates surfactant homeostasis and attenuates cardiopulmonary injury in a context-dependent manner. These findings support further investigation into SP-D as a component of multimodal severity stratification in OSA and highlight Gal-3 inhibition as a context-dependent anti-inflammatory strategy, pending validation in larger cohorts with tissue-level confirmation.

Background: Respiratory diseases remain a major contributor to mortality in Europe, yet national long-term analyses rarely explore sex- and age-specific temporal patterns in detail. Large international datasets provide aggregated estimates but may obscure country-specific trend changes relevant for public health planning. The aim of the study was to assess long-term trends in mortality from chronic lower respiratory diseases (ICD-10: J40-J47) as well as pneumonia and influenza. (ICD-10: J10-J18) in Poland, with particular emphasis on sex- and age-specific trajectories and joinpoint-defined changes over time. Methods: All deaths among Polish residents aged &#x2265;65 years were analysed using nationwide mortality registry data. Age-standardised death rates (SDRs) were calculated, and temporal trends were assessed using joinpoint regression models to estimate annual percentage changes (APC) and average annual percentage change (AAPC). Results: The proportion of deaths attributable to respiratory diseases increased in both men and women across early (65-74 years) and late (&#x2265;75 years) old age. Mortality from chronic lower respiratory diseases declined throughout the study period among men, with the most pronounced reductions observed in the early 2000s, particularly among those aged &#x2265;75 years, while trends among women remained largely stable or showed only gradual declines. In contrast, mortality from pneumonia and influenza rose markedly across all sex and age subgroups, with distinct trend reversals observed after 2008-2009. Conclusions: Long-term respiratory mortality trends in Poland exhibit marked sex- and age-specific differences that are not fully captured by aggregated international analyses. These findings highlight the importance of country-level, stratified assessments when interpreting respiratory mortality patterns and underscore the need for caution when relying on single time-point indicators for risk assessment and policy planning.

Anti-melanoma differentiation-associated gene 5 (anti-MDA5) antibody-positive interstitial lung disease (ILD) is associated with high mortality. While inflammatory markers have been linked to poor outcomes, clinical heterogeneity remains evident, as some patients survive despite marked hyperinflammation. We retrospectively analyzed consecutive patients with anti-MDA5 antibody-positive ILD treated at our institution between May 2017 and November 2025. In-hospital mortality was assessed in relation to clinical characteristics and laboratory markers, including peak anti-MDA5 antibody titers, ferritin, C-reactive protein (CRP), lactate dehydrogenase (LDH), and KL-6. Analyses were exploratory and hypothesis-generating. Continuous variables were compared using Mann-Whitney U tests, and categorical variables using Fisher's exact test. Principal component analysis (PCA) and receiver operating characteristic (ROC) analyses were performed for descriptive purposes. Seventeen patients were included (10 survivors and 7 non-survivors). Peak ferritin, C-reactive protein (CRP), and lactate dehydrogenase (LDH) levels were significantly higher in non-survivors, whereas peak anti-MDA5 antibody titers showed a non-significant trend toward higher values in non-survivors (p = 0.057). KL-6 levels did not differ significantly between groups. In ROC analyses, LDH and CRP showed the highest discriminative performance for in-hospital mortality, followed by ferritin, whereas KL-6 showed the lowest discriminative performance. Despite these overall trends, substantial overlap between survivors and non-survivors remained across all biomarkers. Principal component analysis (PCA) demonstrated partial separation of outcomes along an inflammation-dominant axis, but with persistent overlap, indicating marked outcome heterogeneity. Inflammatory biomarkers, particularly LDH, CRP, and ferritin, were associated with in-hospital mortality in anti-MDA5 antibody-associated ILD. However, persistent overlap between survivors and non-survivors suggests that single-biomarker assessment is insufficient for precise prognostication. These findings should be interpreted as hypothesis-generating and require validation in larger multicenter cohorts.

(1) Background: Innate lymphoid cells (ILCs) are potent cytokine producers that regulate local immune responses in tissues. Natural killer (NK) cells belong to group 1 ILCs and play an important role in tumor clearance and defense against intracellular pathogens. ILC2 and 3 have been implied in allergic responses and other chronic inflammatory diseases. The role of these cells in the pathogenesis of chronic rhinosinusitis (CRS) is not completely understood. There are changes in the cellular infiltrate in the mucosa of patients with CRS with and without polyps. The aim of this study was to characterize the number and phenotype of NK cells, ILC2s and ILC3s in patients with CRS. (2) Methods: Tissue samples were collected from patients with CRS with and without nasal polyps who were undergoing nasal sinus surgery as well as control patients who were undergoing surgery due to non-inflammatory reasons. Lymphocytes were isolated from the tissues using mechanical and enzymatic dissociation. Peripheral blood lymphocytes were obtained from the same patients. All cells were examined by multicolor flow cytometry. NK cells were analyzed for the distribution of CD56dimCD16+ and CD56brightCD16- subsets and the expression of IL18R&#x3b1;, CD16, CD57, GATA3, TCF1 and NKp44. In ILC2s, GATA3 and IL18R&#x3b1; expression was determined, and ILC3s as well as NKp44+ and NKp44-ILC3 subsets were analyzed for the expression of IL18R&#x3b1;. (3) Results: There were significantly fewer NK cells in the nasal polyps compared to the peripheral blood of patients with CRSwNP and tissues from CRSsNP patients, which both showed higher levels of TCF1 expression. Irrespective of the disease condition, NK cells in tissues showed lower CD16 expression and a lower frequency of the CD56dimCD16+ subset compared to the peripheral blood mononuclear cells. Additionally, a smaller percentage of NK cells were terminally matured, as measured by CD16+ and CD57+ expression, in all examined nasal mucosa tissues. In the tissue ILC3s, we predominantly found cells from the NKp44- subset in all groups. ILC3s from CRSsNP patients showed the highest frequencies of IL18R&#x3b1;+ cells of all examined tissues. ILC2s from the polyps ofCRSwNP patients showed higher levels of GATA3 expression than their peripheral blood counterparts. (4) Conclusions: We found that tissue-resident NK cells in mucosa from the nose and sinuses are a more heterogenous and less mature population than those in peripheral blood. Expression of the examined markers in NK cells was similar among groups. NK cell frequency, both in blood and tissue from CRSsNP patients, was higher than in the other groups, indicating that these cells might play an important role in this phenotype. Changes in the IL18R&#x3b1; expression of ILC3s suggest a potential role of IL18 signaling in CRS pathogenesis.

Pneumoconiosis remains a major occupational lung disease associated with progressive respiratory impairment, reduced functional capacity, and diminished quality of life. Non-pharmacological rehabilitation has been increasingly proposed as a supportive intervention; however, evidence regarding its effectiveness remains heterogeneous. This study aimed to systematically review and synthesize the available evidence on the effects of non-pharmacological rehabilitation interventions on functional capacity, quality of life, and psychological outcomes in patients with pneumoconiosis. A systematic literature search was conducted in major electronic databases and grey literature sources in accordance with PRISMA 2020 guidelines. Studies evaluating non-pharmacological rehabilitation interventions in adults with pneumoconiosis were eligible for inclusion. Outcomes of interest included functional capacity, health-related quality of life, and psychological well-being. Due to methodological heterogeneity across studies, a qualitative synthesis was performed. Six studies met the predefined inclusion criteria and were included in the qualitative synthesis. The reviewed evidence suggests that structured rehabilitation interventions were associated with clinically meaningful improvements in functional capacity, particularly in structured rehabilitation programs, most consistently reflected by increases in six-minute walk distance exceeding established minimal clinically important differences in three studies. Improvements in health-related quality of life and selected psychological outcomes were also reported, although outcome measures and intervention protocols varied across studies. Significant improvements in exercise capacity, dyspnea severity, and health-related quality of life were reported. Non-pharmacological rehabilitation may provide clinically meaningful benefits for patients with pneumoconiosis, based on limited and heterogeneous evidence, particularly in terms of functional capacity and quality of life. Nevertheless, the current evidence base is limited by heterogeneity in study design and outcome reporting. Further high-quality, standardized trials are needed to strengthen the evidence and guide the clinical implementation of rehabilitation programs for occupational lung diseases.

Introduction: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality. Early identification and timely intervention for COPD exacerbations can reduce hospitalizations and complications, as well as improve patient outcomes. Methods: To develop and evaluate predictive models for COPD exacerbations using machine learning (ML), we performed a retrospective study using intensive care unit patient records. Records including 31,667 clinical notes and 10,489 vital signs were used to train and validate two machine learning models to predict COPD exacerbations in patients with known or suspected COPD. Predictive performance was evaluated for support vector machine, quadratic discriminant analysis, and adaptive boosting algorithms using area under the receiver operating characteristic curve (AUC). Results: The clinical note-based support vector machine model achieved an AUC of 0.81 and accuracy of 84.0% in predicting COPD exacerbations. Data from patient monitors and hospital information systems provided sufficient information for accurate prediction, demonstrating the utility of combining physiological signals with clinical text data. Discussion: Clinically available patient data and vital signs can effectively predict COPD exacerbations, potentially enabling earlier interventions, improved outcomes, and reduced healthcare burden. These findings suggest that integrating unstructured clinical notes with structured vital signs using ML frameworks may improve early detection of exacerbation risk, thus enabling appropriate patient counseling, triage, and treatment based on COPD severity.

Dysfunctional breathing patterns may impair autonomic regulation and increase perceived stress. Breathing-based interventions, particularly those involving guided exercises and supportive tools, have the potential to provide non-pharmacological benefits. In this parallel two-arm randomized controlled trial, 14 women aged 35-45 years with signs of dysfunctional breathing and no comorbidities were recruited from a fitness club. Participants were randomly assigned (1:1) using a computer-generated sequence to an intervention group (n = 7) or a control group (n = 7). Blinding was not applied. Both groups completed a 6-week program of guided breathing exercises using the iBreathe app, while the intervention group additionally used mouth tape during sleep. The primary outcomes were heart rate variability (HRV) indices-root mean square of successive differences (RMSSD) and the high-frequency (HF) component. Secondary outcomes included respiratory rate, Hencho test performance, and perceived stress measured using the Perceived Stress Scale-10 (PSS-10) and a Visual Analogue Scale (VAS). All participants were included in the final analysis (no loss to follow-up). The intervention group showed a significant increase in the HF component of HRV (p = 0.018) and improved Hencho test performance (p = 0.018). Both groups demonstrated significant reductions in respiratory rate (p < 0.05) and PSS scores (p < 0.05). Between-group differences were not significant for RMSSD or perceived stress. No adverse events were reported. A 6-week breathing intervention improved respiratory efficiency and reduced perceived stress among women with dysfunctional breathing. The additional of night-time mouth taping provided further benefits for HRV and respiratory control. Larger and longer trials are needed to confirm these findings.

Background: Highly effective CFTR modulation with Elexacaftor/Tezacaftor/Ivacaftor (ETI) markedly improves clinical outcomes in people with cystic fibrosis (CF). Data on its effects on physical activity, sleep, sinonasal symptoms, and parent-perceived outcomes in preschool-aged children are limited. Methods: In this prospective, observational, single-center cohort study, ten children with cystic fibrosis (aged 2-6 years) and at least one CFTR variant eligible for ETI were included. Data were collected using wrist-worn Garmin v&#xed;vofit Junior 2 activity trackers and standardized questionnaires one month before ETI initiation and at 1, 3, 6, and 12 months after start of ETI. Outcomes included step count, minutes of moderate-to-vigorous physical activity, sleep parameters, sinonasal symptoms, and parental perceptions. Results: ETI was well tolerated. Sweat chloride levels decreased significantly. Physical activity improved at 3 and 6 months (step count and active minutes/day; p < 0.05) but declined to near-baseline levels at 12 months. Parental assessments of physical and sporting performance showed sustained improvement. Sleep duration remained stable, with no changes in deep or light sleep phases or nighttime awakenings. Sinonasal symptoms remained low. Discussion & Conclusions: Preliminary findings of this exploratory pilot study show that improvement in physical activity after three and six months of ETI therapy might be attributable to seasonality, as therapy was started in winter months. No changes in sleep duration or sleep patterns are reassuring in this small cohort of young children with CF. ETI therapy was safe and well tolerated. Parental appraisal of their children's physical performance improved after start of ETI. Longitudinal, controlled studies involving larger cohorts are required to validate these findings and to account for potential confounding factors, such as age-dependent changes and individual and environmental factors such as seasonal variation.

Mucopolysaccharidosis (MPS) are a group of inherited lysosomal storage genetic disorders that affect the body's ability to break down glycosaminoglycans (GAGs) due to the deficiency of required enzymes. This leads to depositions of these GAGs in various tissues and organs resulting in multi-systemic manifestations including pulmonary and sleep related issues. In recent years, there have been significant advancements in therapeutic options and supportive management which have led to the overall improvement in respiratory care, culminating in improved quality of life for MPS patients. Management of pulmonary and sleep disorders in mucopolysaccharidosis requires a multidisciplinary approach due to the multi-systemic affectation of the genetic disorders. Therapeutic options such as enzyme replacement therapy (ERT) and hematopoietic stem cell transplantation (HSCT) have yielded varying success in mitigating respiratory complications. Emerging treatments such as gene therapies have shown exciting and promising results thus far. Supportive therapies such as airway clearance, regular vaccination and use of positive airway pressure devices are also essential. Pre-operative airway and anesthesia planning is critical to mitigate peri-operative and post-operative complications. Early diagnosis, close monitoring and a patient focused individualized approach are essential for respiratory optimization and overall improvement in clinical outcomes. This review article aims to discuss these advancements in a comprehensive format, making it accessible to medical providers who care for this subset of patients.

Objective: Rapid assessment of early treatment-related physiological improvement in emergency department (ED) patients with respiratory failure (RF) remains challenging. Blood gas analysis is informative but invasive and not ideal for repeated use. The vertical displacement index (VDI), an ultrasound-derived parameter based on pleural motion, may provide dynamic bedside information on early physiological change. This study evaluated whether changes in VDI are associated with early physiological improvement in ED patients with RF. Methods: This prospective observational study was conducted in the EDs of two tertiary care hospitals. Adult patients presenting with dyspnea and clinical evidence of RF were included. VDI was measured by lung ultrasound at baseline and 30 min after initial treatment. The primary endpoint was the change in VDI 30 min after the initial treatment, calculated as the difference between pre-treatment and post-treatment VDI. The expected direction was a post-treatment decrease in VDI, with greater VDI reduction expected to be associated with greater early physiological improvement. Secondary analyses included comparisons of VDI changes across oxygen saturation and diagnostic groups, as well as correlations between &#x394;VDI and physiological changes. Patients were grouped by admission oxygen saturation (<80%, 80-90%, and &#x2265;90%). Results: Seventy-nine patients were included. Pre-treatment VDI differed significantly between oxygen saturation groups, with the highest values in the most hypoxemic patients (p = 0.028). VDI decreased significantly after treatment in all groups (p < 0.001 for all), with the greatest reduction in the <80% group. By diagnosis, VDI decreased significantly in pulmonary edema, COPD/asthma, and pneumonia, but not in pulmonary embolism (p = 0.138). VDI reduction correlated positively with improvements in oxygen saturation (r = 0.27, p = 0.016) and pH (r = 0.24, p = 0.037), but not with CO2. Conclusions: VDI may be explored as a practical ultrasound-derived bedside parameter associated with early physiological improvement in ED patients with RF.

Introduction: It is estimated that up to 75% of pregnant women complain of dyspnea at some point during pregnancy. Asthma is the most common chronic pulmonary disease complicating pregnancy. Well controlled asthma does not affect pregnancy negatively. However, asthma exacerbations are linked with several adverse perinatal outcomes. As diligent treatment of asthma significantly reduces the number of asthma exacerbations, it is important to properly detect asthmatic patients among pregnant women in order to provide them with better care. The most efficient way to diagnose asthma is to perform spirometry with a reversibility test. There are no studies that have examined the safety of performing spirometry and, more specifically, a reversibility test, during pregnancy. Objectives: In this systematic review we aimed to review current available data regarding the safety of performing spirometry and a reversibility test during pregnancy. Patients and methods: For this systematic review, we searched PubMed, Scopus and Cochrane databases. We used the following search terms: (pregnancy); (spirometry); (lung function test); (pulmonary function test); (reversibility test); (post-bronchodilator challenge); (safety). Results: We collected reports of spirometry performed on pregnant women and analyzed them for complications that occurred during the procedure. Out of 13,594 records identified for the aforementioned search words, we included 78 documents that met the inclusion criteria. In total, the studies consisted of over 33,405 spirometry attempts performed by 10,617 pregnant women. Additionally, the reversibility test was conducted in nine studies. In all of the selected articles, there were no reports of adverse events occurring while performing spirometry. Conclusions: In this systematic review we aimed to summarize the current available data about the safety of performing spirometry during pregnancy. Several studies have investigated pulmonary function tests during pregnancy. No studies reported any adverse events that occurred while performing the procedure. In order to better characterize the safety profile of spirometry, including during pregnancy, further prospective studies systematically reporting on adverse symptoms during spirometry are required.

(1) Background: Pulmonary hypertension (PH) is characterized by respiratory muscle weakness, limited exercise tolerance, and reduced quality of life, but inspiratory muscle training (IMT) has emerged as a potential non-pharmacological strategy to improve functional outcomes in this population. This systematic review and meta-analysis evaluated the effects of isolated IMT on respiratory function, exercise capacity, symptom burden, and safety in adults with PH. (2) Methods: A systematic search was conducted in accordance with PRISMA guidelines. Randomized controlled trials involving adults with PH who underwent isolated IMT were included, and respiratory muscle strength, spirometric parameters, exercise capacity, dyspnea, fatigue, quality of life, and adverse events were the outcomes that were assessed. Data were pooled using meta-analytic techniques where appropriate. (3) Results: A total of 130 participants, assigned to five randomized controlled trials, met the inclusion criteria. IMT significantly improved maximal inspiratory pressure (MD = +24.01 cmH2O), maximal expiratory pressure (MD = +23.64 cmH2O), and six-minute walk distance (MD = +60.61 m), but no significant changes were observed in spirometric indices (FEV1%, FVC%, and FEV1/FVC). While several individual studies demonstrated clinically relevant improvements in six-minute walk distance, the pooled analysis did not demonstrate a statistically significant effect. IMT consistently reduced dyspnea and fatigue and improved quality-of-life domains. No serious adverse events were reported, and adherence was high. (4) Conclusions: IMT is a safe and feasible adjunct intervention in PH, providing meaningful improvements in respiratory muscle strength and symptom burden. Further large-scale trials are warranted to confirm its long-term clinical benefits.

Pulmonary actinomycosis is a rare chronic infection that frequently mimics lung malignancy, often leading to delayed diagnosis due to its non-specific clinical and radiological presentation. Given the diagnostic challenges associated with this condition, the aim of this study was to evaluate the clinical presentation, diagnostic pathways, treatment strategies, and outcomes of patients diagnosed with pulmonary actinomycosis in a single center. We retrospectively reviewed patients diagnosed with pulmonary actinomycosis at our institution between January 2014 and December 2022. Diagnosis was established based on compatible clinical and radiological findings together with microbiological identification of Actinomyces by culture or polymerase chain reaction. Twenty-two patients were included in the final analysis. The median age was 61.5 years and males were more frequently affected (59%). The median time from initial hospitalization to definitive diagnosis was 70 days. Actinomyces odontolyticus was the most frequently identified species. All patients received antibiotic therapy, with a median treatment duration of 45.5 days. Thirteen patients underwent surgical intervention, performed either for diagnostic purposes or for treatment of complications. Complete disease eradication through surgical management was achieved in six cases. During follow-up (median 24 months), overall survival at three years was 78%, with one death directly related to pulmonary actinomycosis. Pulmonary actinomycosis remains a diagnostic challenge due to its non-specific clinical presentation and low microbiological yield. Early clinical suspicion and a combined diagnostic approach including bronchoscopy and microbiological testing are essential for timely diagnosis. Surgical intervention may play an important diagnostic and therapeutic role in selected patients.

Prognostic markers reflecting nutritional vulnerability in idiopathic pulmonary fibrosis (IPF) remain poorly defined. In this prospective cohort study, 63 stable outpatients with IPF were followed for 3 years. Sarcopenia was defined according to the 2019 Asian Working Group for Sarcopenia criteria. Serum transthyretin levels were measured concurrently. Cox proportional hazards regression, binary logistic regression, and Kaplan-Meier survival analyses were performed. During follow-up, 18 patients (29%) died and 21 (33%) experienced respiratory-related hospitalization. Serum transthyretin was an independent predictor of both 3-year mortality and respiratory-related hospitalization, even after adjusting for the Gender-Age-Physiology index. Conversely, sarcopenia and low appendicular skeletal muscle mass index (ASMI) were not independently associated with either outcome. Kaplan-Meier analysis demonstrated significant differences in both mortality and hospitalization according to serum transthyretin levels. Low ASMI evaluated using sex-specific cutoffs was associated with higher mortality in the unadjusted analysis, but not with hospitalization; sarcopenia was not significantly associated with either endpoint. Serum transthyretin may serve as a practical biomarker of nutritional vulnerability, providing complementary prognostic information beyond muscle mass-based assessment in IPF.

Air pollution is a major environmental determinant of respiratory health and a significant contributor to the global burden of childhood asthma. Although several recent narrative and systematic reviews have examined environmental triggers of asthma, highlighting air pollution as a consistent risk factor across diverse populations and study designs, recent epidemiological evidence-including multicenter cohort studies and region-specific analyses from Europe and Greece-has not been systematically synthesized. To systematically review recent epidemiological evidence (2000-2025) on the association between ambient air pollution and childhood asthma incidence and exacerbations, with emphasis on European and Greek populations. Following PRISMA guidelines, we systematically reviewed observational studies published between 2000 and 2025 in PubMed, Scopus, Web of Science, BMC, and Google Scholar. Studies evaluating quantitative exposure to PM2.5, PM10, NO2, O3, or SO2 and asthma incidence, prevalence, or exacerbations in children (&#x2264;18 years) were included. Evidence was synthesized by pollutant type, exposure window, geographic region, and study design. Twenty-four studies involving more than 3.5 million children were included. Consistent associations were observed across international and European cohorts between long-term exposure to PM2.5, PM10, and NO2 and increased asthma incidence. Risk estimates typically ranged from 15% to 30% increases in asthma incidence per 10 &#x3bc;g/m3 increase in long-term exposure to PM2.5 or NO2, as reported across multiple cohort analyses. Early-life exposure showed the strongest effects on asthma development and lung function decline. European and Greek studies demonstrated comparable trends, highlighting increased hospitalizations and symptom burden in urban populations despite pollutant concentrations often below current regulatory thresholds. Short-term pollution peaks were additionally associated with increased asthma exacerbations and hospital admissions, particularly during seasonal episodes of elevated particulate matter and ozone concentrations. This review provides an updated synthesis of 21st-century evidence demonstrating that ambient air pollution is a major and modifiable determinant of childhood asthma. The consistency of findings across regions, combined with limited longitudinal evidence from Greece, highlight the importance of improved air-quality management and continued public-health efforts to reduce exposure and the need for enhanced epidemiological monitoring.

Asthma is characterized by persistent airway epithelial dysfunction and remodelling of the reticular basement membrane (RBM). In healthy airways, the RBM is primarily composed of the extracellular matrix (ECM) proteins laminin and collagen-IV, but in remodelled asthmatic airways, the RBM has increased deposition of collagen-I, -III and fibronectin. Here, we systematically compared the effects of collagen-I, -III, -IV, fibronectin, laminin, and bovine serum albumin (BSA) control on bronchial epithelial cells (BECs) from six healthy controls and seven individuals with asthma. Epithelial attachment, spreading and barrier function were assessed in real time over 72 h using electrical cell-substrate impedance sensing. Cell culture supernatants were analyzed for release of epithelial cytokines, thymic stromal lymphopoietin (TSLP), interleukin (IL)-6, IL-8, and IL-11 using ELISA. BECs from both control and asthma donors had faster cell attachment, spreading, and barrier formation on collagen-I, -III, -IV, and fibronectin compared to laminin and BSA. BECs from both control and asthma donors cultured on collagen -I and -III produced more TSLP, but had no effect on IL-6, IL-8, and IL-11 expression. In summary, remodelling of the RBM in asthma may promote epithelial barrier formation whilst simultaneously enhancing epithelial-derived Th2 inflammation through increased TSLP release.

Chronic respiratory diseases, including chronic obstructive pulmonary disease (COPD), asthma, pneumoconiosis, interstitial lung disease (ILD) and pulmonary sarcoidosis, are major global causes of mortality and morbidity. Although the COVID-19 pandemic has influenced acute respiratory health, its impact on chronic respiratory conditions remains unclear. We estimated the global, regional and national burden of chronic respiratory diseases from 1990 to 2023, including risk factors, and evaluated how these burdens have shifted during the COVID-19 pandemic using the Global Burden of Disease Study 2023. In 2023, chronic respiratory diseases accounted for 569.2 million (95% uncertainty interval (UI), 508.8-639.8) cases and 4.2 million (3.6-5.1) deaths. The age-standardized death rate declined by 25.7% globally from 1990 to 2023 despite an increase in ILD and pulmonary sarcoidosis. Mortality declined in younger males, especially for asthma, whereas older adults experienced a rise in ILD and pulmonary sarcoidosis. Smoking was the primary risk factor for COPD, whereas high body mass index and silica exposure were key risk factors for asthma and pneumoconiosis. During the pandemic, the incidence of chronic respiratory diseases increased modestly, but the decline in mortality rates became more pronounced, highlighting the need for sustained global attention and action to address their long-term burden.

Corisin, a microbiota-derived proapoptotic peptide, has emerged as a key mediator of epithelial injury, inflammation, and acute exacerbation in fibrotic lung disease. Although acute corisin inhibition prevents exacerbations in experimental models, its therapeutic impact on established pulmonary fibrosis remains unclear. This study evaluated the short-term efficacy of corisin neutralization in advanced transforming growth factor-&#x3b2;1 (TGF-&#x3b2;1)-driven lung fibrosis. Male TGF-&#x3b2;1 transgenic mice with established fibrosis were allocated to computed tomography-matched groups and treated intraperitoneally with an anti-corisin monoclonal antibody (clone 21A) or control IgG every two days for one week. Bronchoalveolar lavage fluid (BALF) analysis, histopathology, assessment of apoptosis, Ashcroft scoring, and lung hydroxyproline quantification were performed on day 8. Anti-corisin treatment significantly reduced BALF inflammatory cell counts, including macrophages and lymphocytes. Histological analyses demonstrated decreased alveolar epithelial apoptosis, reduced collagen deposition, and significantly lower Ashcroft fibrosis scores. Lung hydroxyproline content was also markedly decreased, indicating attenuation of extracellular matrix accumulation. Short-term neutralization of microbiota-derived corisin rapidly alleviates inflammation, epithelial injury, and fibrotic remodeling in advanced TGF-&#x3b2;1-induced pulmonary fibrosis. These findings identify corisin as an upstream driver of ongoing fibrogenesis and support its potential as a therapeutic target in progressive fibrotic lung disease.