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Background Rhinovirus infections commonly evoke asthma exacerbations in children and adults. Recurrent asthma exacerbations are associated with injury-repair responses in the airways that collectively contribute to airway remodeling. The physiological consequences of airway remodeling can manifest as irreversible airway obstruction and diminished responsiveness to bronchodilators. Structural cells of the airway, including epithelial cells, smooth muscle, fibroblasts, myofibroblasts, and adjacent lung vascular endothelial cells represent an understudied and emerging source of cellular and extracellular soluble mediators and matrix components that contribute to airway remodeling in a rhinovirus-evoked inflammatory environment. Main body While mechanistic pathways associated with rhinovirus-induced airway remodeling are still not fully characterized, infected airway epithelial cells robustly produce type 2 cytokines and chemokines, as well as pro-angiogenic and fibroblast activating factors that act in a paracrine manner on neighboring airway cells to stimulate remodeling responses. Morphological transformation of structural cells in response to rhinovirus promotes remodeling phenotypes including induction of mucus hypersecretion, epithelial-to-mesenchymal transition, and fibroblast-to-myofibroblast transdifferentiation. Rhinovirus exposure elicits airway hyperresponsiveness contributing to irreversible airway obstruction. This obstruction can occur as a consequence of sub-epithelial thickening mediated by smooth muscle migration and myofibroblast activity, or through independent mechanisms mediated by modulation of the β 2 agonist receptor activation and its responsiveness to bronchodilators. Differential cellular responses emerge in response to rhinovirus infection that predispose asthmatic individuals to persistent signatures of airway remodeling, including exaggerated type 2 inflammation, enhanced extracellular matrix deposition, and robust production of pro-angiogenic mediators. Conclusions Few therapies address symptoms of rhinovirus-induced airway remodeling, though understanding the contribution of structural cells to these processes may elucidate future translational targets to alleviate symptoms of rhinovirus-induced exacerbations.

COPD is characterized by chronic bronchitis, chronic airway obstruction, and emphysema, leading to a progressive and irreversible decline in lung function. Inflammation is central for the development of COPD. Chronic inflammation in COPD mainly involves the infiltration of neutrophils, macrophages, lymphocytes, and other inflammatory cells into the small airways. The contribution of resident airway structural cells to the inflammatory process is also important in COPD. Airway remodeling consists of detrimental changes in structural tissues and cells including airway wall thickening, epithelial metaplasia, goblet cell hypertrophy, and smooth muscle hyperplasia. Persistent airway inflammation might contribute to airway remodeling and small airway obstruction. However, the underlying mechanisms remain unclear. In this review, we will provide an overview of recent insights into the role of major immunoinflammatory cells in COPD airway remodeling.

Introduction Central airway obstruction (CAO) represents a pathological condition that can lead to airflow limitation of the trachea, main stem bronchi , bronchus intermedius or lobar bronchus . Main body It is a common clinical situation consensually considered under-diagnosed. Management of patients with CAO can be difficult and deciding on the best treatment approach represents a medical challenge. This work intends to review CAO classifications, causes, treatments and its therapeutic limitations, approaching benign and malign presentations. Three illustrative cases are further presented, supporting the clinical problem under review. Conclusion Management of CAO still remains a challenge. The available options are not always effective nor free from complications. A new generation of costume-tailored airway stents, associated with stem cell-based therapy, could be an option in specific clinical situations.

Background Originally, studies on exhaled droplets explored properties of airborne transmission of infectious diseases. More recently, the interest focuses on properties of exhaled droplets as biomarkers, enabled by the development of technical equipment and methods for chemical analysis. Because exhaled droplets contain nonvolatile substances, particles is the physical designation. This review aims to outline the development in the area of exhaled particles, particularly regarding biomarkers and the connection with small airways, i e airways with an internal diameter < 2 mm. Main body Generation mechanisms, sites of origin, number concentrations of exhaled particles and the content of nonvolatile substances are studied. Exhaled particles range in diameter from 0.01 and 1000 μm depending on generation mechanism and site of origin. Airway reopening is one scientifically substantiated particle generation mechanism. During deep expirations, small airways close and the reopening process produces minute particles. When exhaled, these particles have a diameter of < 4 μm. A size discriminating sampling of particles < 4 μm and determination of the size distribution, allows exhaled particle mass to be estimated. The median mass is represented by particles in the size range of 0.7 to 1.0 μm. Half an hour of repeated deep expirations result in samples in the order of nanogram to microgram. The source of these samples is the respiratory tract ling fluid of small airways and consists of lipids and proteins, similarly to surfactant. Early clinical studies of e g chronic obstructive pulmonary disease and asthma, reported altered particle formation and particle composition. Conclusion The physical properties and content of exhaled particles generated by the airway reopening mechanism offers an exciting noninvasive way to obtain samples from the respiratory tract lining fluid of small airways. The biomarker potential is only at the beginning to be explored.

Various therapeutic bronchoscopy techniques, including stenting, are widely utilized in the treatment of malignant central airway obstruction (MCAO), however, little data exist on the independent clinical outcomes and prognostic factors of airway stenting on MCAO. We retrospectively analyzed 287 eligible patients with MCAO who underwent therapeutic bronchoscopy at the Department of Pulmonary and Critical Care Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, between January 1, 2016, and May 31, 2023. The length of survival was measured in months from the date of the first bronchoscopy procedure to the date of death, or until six months post-procedure or loss to follow-up. Dyspnea was assessed using the Borg score, modified Medical Research Council (mMRC), and 6-minute walk distance (6MWD), while quality of life (QoL) was evaluated using the Short Form 6-Dimension (SF-6D) and Karnofsky Performance Status (KPS) score. All assessments were conducted consecutively at baseline, three months, and six months following the procedure. The overall survival rate was illustrated using the Kaplan-Meier curve, and the Cox proportional hazards mode were applied to evaluate multiple prognostic factors affecting survival in both groups over a 6-month follow-up period. A total of 287 patients were analyzed, including 215 in the stent group and 72 in the non-stent group. A significant difference in lesion location was observed between the groups. Postoperative stenosis was significantly improved in the stent group, with 94.41% achieving grade I stenosis compared to 8.33% in the non-stent group ( P = 0.001). The stent group also showed greater improvements in KPS, Borg scores, SF-6D, and 6MWD compared to the non-stent group ( P = 0.001). Additionally, significant improvements in Borg score, mMRC, 6MWD, KPS, and SF-6D were maintained at three- and six-month follow-ups. The mean survival period was significantly longer in the stent group (5.1 months) compared to the non-stent group (4.6 months). The Cox proportional hazards model identified the type of stenosis (HR: 0.184, 95% CI: 0.047–0.968, P = 0.015) and the degree of stenosis after the procedure (HR: 0.211, 95% CI: 0.061–0.726, P = 0.014) as significant factors influencing survival outcomes. Airway stenting is a safe and effective procedure leading to significant improvements in clinical symptoms and QoL for patients with MCAO at a 6-month follow-up. The type and severity of stenosis were identified as significant prognostic factors for survival.

Purpose Pressure support is often used for extubation readiness testing, to overcome perceived imposed work of breathing from endotracheal tubes. We sought to determine whether effort of breathing on continuous positive airway pressure (CPAP) of 5 cmH 2 O is higher than post-extubation effort, and if this is confounded by endotracheal tube size or post-extubation noninvasive respiratory support. Methods Prospective trial in intubated children. Using esophageal manometry we compared effort of breathing with pressure rate product under four conditions: pressure support 10/5 cmH 2 O, CPAP 5 cmH 2 O (CPAP), and spontaneous breathing 5 and 60 min post-extubation. Subgroup analysis excluded post-extubation upper airway obstruction (UAO) and stratified by endotracheal tube size and post-extubation noninvasive respiratory support. Results We included 409 children. Pressure rate product on pressure support [100 (IQR 60, 175)] was lower than CPAP [200 (120, 300)], which was lower than 5 min [300 (150, 500)] and 60 min [255 (175, 400)] post-extubation (all p  < 0.01). Excluding 107 patients with post-extubation UAO (where pressure rate product after extubation is expected to be higher), pressure support still underestimated post-extubation effort by 126–147 %, and CPAP underestimated post-extubation effort by 17–25 %. For all endotracheal tube subgroups, ≤3.5 mmID ( n  = 152), 4–4.5 mmID ( n  = 102), and ≥5.0 mmID ( n  = 48), pressure rate product on pressure support was lower than CPAP and post-extubation (all p  < 0.0001), while CPAP pressure rate product was not different from post-extubation (all p  < 0.05). These findings were similar for patients extubated to noninvasive respiratory support, where pressure rate product on pressure support before extubation was significantly lower than pressure rate product post-extubation on noninvasive respiratory support ( p  < 0.0001, n  = 81). Conclusions Regardless of endotracheal tube size, pressure support during extubation readiness tests significantly underestimates post-extubation effort of breathing.

ObjectivesPulmonary function impairment and chronic respiratory symptoms after tuberculosis are relatively common in low-income and middle-income countries. We aimed to estimate the impact of post-tuberculosis (post-TB) on pulmonary function.MethodsThis large cross-sectional, population-based study included subjects aged 15 years or older with technically acceptable postbronchodilator spirometry measurements. Post-TB was diagnosed on the basis of radiological evidence and/or medical history. Airflow obstruction was defined as a postbronchodilator forced expiratory volume in 1 s/forced vital capacity ratio below the lower limit of normal of Global Lung Function Initiative (GLI) lung function equations. Small airway dysfunction was diagnosed if at least two of the following indicators were less than 65% of predicted: maximal mid-expiratory flow, forced expiratory flow (FEF) 50% or FEF 75%.ResultsIn this population sample (N=8680, mean age: 40.1 years), 610 (7.0% (95% CI 6.5 to 7.6) participants were post-TB. Post-TB subjects had more frequent respiratory symptoms (46.8% vs 28.3%). Among post-TB subjects, 130 (21.3% (95% CI 18.1 to 24.8)) had airflow obstruction; OR of airflow obstruction was significantly associated with post-TB after adjustment for other confounding factors (OR 1.31, 95% CI 1.05 to 1.62). Post-TB was also associated with small airway dysfunction (OR 1.28, 95% CI1.07 to 1.53), which was present in 297 (48.9% (95% CI 33.9 to 53.0)) post-TB subjects.ConclusionsOur findings support existing knowledge that post-TB is positively associated with pulmonary function impairment and make for frequent respiratory symptoms. Post-TB should be considered as a potentially important cause of airflow obstruction and respiratory symptoms in patients originating from countries with a high burden of tuberculosis.

Failure to establish an airway can be life-threatening. Although relatively rare, such cases tend to be underreported. Advances in visualization techniques may be helpful. Difficult intubation can often be anticipated and prepared for.

Airway epithelial cells are the first line of defense against the constituents of the inhaled air, which include allergens, pathogens, pollutants, and toxic compounds. The epithelium not only prevents the penetration of these foreign substances into the interstitium, but also senses their presence and informs the organism's immune system of the impending assault. The epithelium accomplishes the latter through the release of inflammatory cytokines and chemokines that recruit and activate innate immune cells at the site of assault. These epithelial responses aim to eliminate the inhaled foreign substances and minimize their detrimental effects to the organism. Quite frequently, however, the innate immune responses of the epithelium to inhaled substances lead to chronic and high level release of pro-inflammatory mediators that may mediate the lung pathology seen in asthma. The interactions of airway epithelial cells with allergens will be discussed with particular focus on interactions-mediated epithelial release of cytokines and chemokines and their role in the immune response. As pollutants are other major constituents of inhaled air, we will also discuss how pollutants may alter the responses of airway epithelial cells to allergens.

Foreign body airway obstruction (FBAO) is a common medical emergency; however, few studies of life-threatening FBAO have been reported and no standard classification system is available. We retrospectively evaluated patients who presented to the emergency departments of two hospitals and were diagnosed with FBAO. The primary outcome was cerebral performance category (CPC) score at discharge. To establish a new classification system for FBAO, FBAO was classified into three types based on the anatomical and physiological characteristics of the obstructed airway. A total of 137 patients were enrolled. Median age was 79.0 years. The most common cause of FBAO was meat, followed by bread, rice cake, and rice. Of all patients, 65.7% suffered cardiac arrest and 51.1% died. In contrast, 28.5% had favorable neurological outcomes, defined as CPC 1 and 2. Upper airway obstruction (type 1) was the most common (type 1, 78.1%), while trachea and/or bilateral main bronchus obstruction (type 2, 12.4%) showed significantly higher mortality than type 1 obstruction (82.4% vs 47.7%, P = 0.0078). Patients with unilateral bronchus and/or distal bronchus obstruction (type 3, 9.5%) were significantly more likely to consume a dysphagia diet than type 1 patients (23.1% vs 0%, P < 0.0001). The majority of patients with life-threatening FBAO were elderly and had poor neurological outcomes. Our new classification system divides FBAO into three types, and revealed that mortality was significantly higher with type 2 than type 1 obstruction. This classification system may improve the management of patients with FBAO and assessment of patient outcomes.