European Respiratory Review最新文献

Background: COPD is associated with an increased risk of infections, such as herpes zoster, potentially leading to greater morbidity and mortality. This systematic review assessed the evidence on herpes zoster burden in COPD.

Methods: A global systematic literature review and meta-analysis was conducted (MEDLINE/Embase, 2003-2024) on herpes zoster burden (incidence, risk, complications, impact on COPD and healthcare resources) in adults aged ≥18 years with COPD.

Results: 22 studies on herpes zoster burden in COPD were included. The pooled herpes zoster incidence rate per 1000 person-years in adults with COPD aged ≥18 years was 10.98 (95% CI 8.28-14.56), increasing to 13.95 (10.80-18.02) in adults aged ≥50 years. The pooled risk ratio of developing herpes zoster was 1.49 (1.17-1.89) in adults aged ≥18 years with COPD and 1.86 (1.28-2.69) in COPD treated with corticosteroids. The pooled rate ratio of developing post-herpetic neuralgia (persistent pain lasting ≥90 days) was 1.50 (1.10-2.04) in adults with herpes zoster and COPD versus with herpes zoster alone. Herpes zoster was linked to higher healthcare costs and resource use, and may be associated with COPD exacerbations. Study designs, settings, case definitions, sample sizes and study periods differed, resulting in heterogeneity.

Conclusions: Adults with COPD have an increased risk of herpes zoster and complications and an associated burden on healthcare systems, with higher risks in those on corticosteroids. Herpes zoster vaccines offer effective protection, including for adults with COPD, and could help reduce the disease and its economic burden.

The lungs are innervated by both afferent and efferent nerve fibres that regulate key respiratory functions, including the cough reflex, airway tone, mucus secretion, and the detection of mechanical and chemical stimuli. In asthma, airway hyperresponsiveness and inflammation are, in part, modulated by the nervous system. Recent findings have identified neuroplasticity as a pathological feature of severe asthma, suggesting that altered neural remodelling contributes to disease symptoms. Additionally, growing evidence highlights bidirectional interactions between the airway nervous system and local immune cells, which play a crucial role in modulating each other's activity. In this review, we explore the emerging roles of airway neuroplasticity and neuroimmune interactions in the development of type 2 inflammation in asthma. We focus on the involvement of neuropeptides and cytokines in mediating this bidirectional crosstalk, aiming to elucidate the mechanistic link between neural remodelling and immune activation and to identify novel targets for pharmacological intervention.

The adult lung is continuously exposed to environmental insults such as pathogens, pollutants and toxins, necessitating robust regenerative mechanisms to maintain tissue integrity and function. Epithelial regeneration relies on the activity and plasticity of resident stem and progenitor cell populations that are spatially distributed across airway and alveolar compartments. Basal cells in the conducting airways and alveolar type (AT) 2 cells in the alveoli act as regional stem cells, capable of self-renewal and multilineage differentiation. Additionally, variant club cells, bronchioalveolar stem cells (BASCs) and newly identified secretory and transitional cell types such as respiratory airway secretory and AT0 cells have emerged as critical players in lung repair. Cellular plasticity, the ability of differentiated cells to dedifferentiate or transdifferentiate, enables rapid adaptation to injury but may also contribute to chronic lung disease when dysregulated. Ageing and chronic injury reduce regenerative capacities, leading to failed repair, fibrotic remodelling or epithelial simplification, as seen in diseases such as idiopathic pulmonary fibrosis and COPD. Recent advances in single-cell and spatial transcriptomics have revealed cellular heterogeneity, novel progenitor states and transitional intermediates that underpin both normal repair and disease pathogenesis. In this review, we integrate findings from animal models and human lung studies to highlight conserved and divergent mechanisms governing cell fate decisions. We discuss how niche signals, transcriptional programmes and extrinsic cues shape epithelial regeneration and explore the therapeutic implications of targeting epithelial plasticity in chronic lung disease.

The lung may be the organ whose mechanical environment needs to be most finely tuned to achieve optimal function. These needs have to be fulfilled at multiple scales, from proper force transmission between the chest wall and the parenchyma to reduction of surface tension by surfactants inside the alveoli. In addition, a plethora of mechanical loads and forces takes place within the lung, from the passive stretch withstood by epithelial cells lining the alveoli, to active forces generated by smooth muscle cells to control airway calibre or cilia beating by ciliary cells in the bronchi to clear debris. Furthermore, the acellular structures in the lung are finely tuned in composition and mechanical properties, from the viscoelastic properties of the mucus to trap pathogens, to the collagen- and elastin-rich extracellular matrix that enables the lung to display elastic recoil at resting volumes but stiffen as it approaches total lung capacity. In this review, we describe the mechanical interplay between the cell types found in the lung, as well as cellular responses to their mechanical niche. We further describe how these responses are altered in diseases such as asthma, COPD, pulmonary fibrosis and lung cancer. In addition, key proteins in mechanotransduction events are detailed, stressing their potential role as therapeutical targets for lung diseases. Finally, we also include a sex perspective to lung pathologies and highlight engineered model systems that may be used to advance our understanding of mechanical forces in experimental investigations or towards lung regeneration.

Background: Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterised by progressive accumulation of surfactant-derived lipoproteinaceous material within alveoli, impairing gas exchange and causing respiratory insufficiency. Despite therapeutic advances such as whole lung lavage, substantial heterogeneity persists in outcome selection and reporting across studies, limiting comparability and evidence synthesis.

Objective: To systematically map and categorise outcomes and outcome measures reported in studies of PAP treatments and establish a foundation for developing a standardised core outcome set (COS).

Methods: A scoping review was conducted across four databases and two clinical trial registries (May 2024, updated May 2025). Eligible studies included those reporting treatment outcomes in patients of any age with PAP. Outcomes and measures were extracted and categorised using the Core Outcome Measures in Effectiveness Trials taxonomy.

Results: From 8475 screened records, 62 studies met the inclusion criteria, encompassing 31 distinct outcomes and 92 corresponding outcome measures. Physiological parameters dominated reporting, including arterial oxygenation (n=55, 89%; such as arterial oxygen tension and alveolar-arterial oxygen gradient) and lung function indices (n=53, 85%; such as diffusing capacity of the lung for carbon monoxide and forced vital capacity) were most frequently assessed. In contrast, patient-centred outcomes such as quality of life were reported in only 10 (16%) studies, while adverse events were relatively well-reported (n=41, 66%).

Conclusions: The reporting of outcomes and outcome measures in PAP studies is highly variable. There is an urgent need for a COS tailored to PAP that focuses on physiological outcomes, adverse events and patient-reported outcomes.

Tuberculosis (TB) primarily manifests as pulmonary TB (PTB), but extrapulmonary TB (EPTB) remains a major clinical challenge. Distinct diagnostic and therapeutic difficulties arise from differences in immune responses, pathogen behaviour and host susceptibility. However, the factors driving disease localisation are still incompletely understood. We conducted a comprehensive narrative review of studies examining differences between PTB and EPTB in terms of epidemiology, mycobacterial factors, genetic and epigenetic determinants, host immune responses, transcriptomic profiles, cytokine and chemokine patterns, and immunophenotypes. EPTB is more common among females, children, older adults and immunocompromised individuals with deficient granuloma formation. This review is intended to provide deeper insight for clinicians and researchers and provides an accessible synthesis of current basic science findings together with their relevance for clinical practice. Certain Mycobacterium tuberculosis lineages, notably lineage 1, and specific virulence factors are associated with extrapulmonary dissemination. While genetic polymorphisms influence TB localisation, no studies specifically addressing epigenetic predisposition to EPTB were identified. PTB typically is characterised by T-helper 1-driven immunity, high bacillary loads and robust macrophage activation, whereas EPTB involves compartmentalised immune responses, reduced cytotoxicity and broader cytokine variability. Transcriptomic analyses reveal site-specific gene expression differences and emerging diagnostic blood-based biomarkers show promise but require further validation. Cytokine profiles and immunophenotyping suggest greater immune exhaustion and regulatory T-cell activity in EPTB. We outline practical implications for diagnosis and management and highlight constraints in resource-limited settings and emphasise access and implementation considerations. Integrating these clinical and mechanistic insights can guide more timely recognition and tailored care.

Background: Ultrafine particles (≤100 nm diameter) may have a higher toxicity than larger particles but are still not regulated nor part of routine air pollution monitoring. So far, health effects of long-term exposure to ambient ultrafine particles are not well understood, owing to a lack of exposure data and epidemiological studies.

Methods: We conducted a systematic review and meta-analysis on the health effects of long-term exposure to ultrafine particles, including studies published until December 2024. A meta-analysis was conducted for outcomes with at least four available effect estimates. Confidence in the body of evidence was evaluated using the Office of Health Assessment and Translation method.

Results: We identified 85 studies investigating various mortality, morbidity and subclinical outcomes. In meta-analyses of single-pollutant models, we found positive associations with natural mortality (hazard ratio 1.06, 95% CI 1.04-1.08) and C-reactive protein (10.14% increase (95% CI -0.51-21.99%) per 10 000 pt·cm^-3 increase in long-term exposure to ultrafine particles, with low and inadequate levels of evidence, respectively. The remaining studies revealed overall limited evidence for adverse effects on a wide range of outcomes. Less than half of the studies adjusted for co-pollutants.

Conclusion: The evidence base on long-term health effects of ultrafine particles has increased substantially in the past decade, while the overall evidence for independent effects of long-term ultrafine particle exposure remains inadequate to low. More studies are needed to draw firm conclusions about the independent adverse effects of long-term ultrafine particles on various health end-points, with a special focus on the influence of co-pollutant adjustment.