Chronic obstructive pulmonary disease (COPD) is a heterogeneous disorder in which spirometry reflects airflow limitation but incompletely captures the underlying structural injury. Patients with similar spirometric impairment may have markedly different patterns of emphysema, small-airway disease, and pulmonary vascular involvement. Computed tomography (CT) can visualize these abnormalities in vivo and may detect structural changes before overt airflow limitation develops. This narrative review examined whether CT-derived imaging markers provide clinically meaningful information beyond spirometry, particularly for phenotyping, early structural detection, prognostic enrichment, and selective clinical decision support. A focused narrative review of diverse publications in PubMed, published between January 2000 and April 2025, was conducted using COPD-related MeSH terms and free-text keywords. Across the reviewed literature, emphysema, quantified by low-attenuation area and emphysema index, and air-trapping measures showed consistent associations with expiratory volume measures and identified structural abnormalities in symptomatic smokers with preserved spirometry. Airway wall metrics such as wall area percentage distinguished airway-predominant phenotypes and were associated with airflow limitation and chronic bronchitis. CT vascular markers, including small-vessel cross-sectional area and the pulmonary artery-to-aorta ratio, reflected microvascular disease; a pulmonary artery enlargement to aorta ratio greater than 1 independently predicted severe exacerbations. Xenon CT and dual-energy CT added regional ventilation and perfusion information but remain investigational. CT imaging markers add complementary structural, phenotypic, and prognostic information beyond spirometry for established COPD and pre-COPD. Their most supported current role is phenotypic characterization and prognostic enrichment in selected clinical settings, whereas advanced functional CT techniques remain research tools. Routine CT for all patients is not supported by current Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidance.

Background: Refractory chronic cough (RCC) is a heterogeneous condition in which clinical phenotyping is used to guide treatment, yet its relationship to the underlying airway pathology remains poorly defined. This study assessed the concordance between clinically defined cough phenotypes and histopathological endotypes derived from bronchial biopsy and bronchoalveolar lavage fluid (BALF) in patients with RCC and compared chest computed tomography (CT) findings across endotypes. Methods: A prospective cross-sectional study was conducted in the cough centre between 2021 and 2025. Adults with RCC lasting more than six months and unresponsive to at least two pharmacological attempts underwent clinical phenotyping (eosinophilic, chronic bronchitis-related, or other) based on clinical symptoms, comorbidities, chest CT, spirometry, FeNO and blood eosinophil count with the assumption that clinical phenotypes might overlap. Histopathological endotype (eosinophilic, neutrophilic, mixed inflammatory, or normal) was assigned based on histopathological assessment of bronchial biopsy and BALF analysis. Results: A total of 30 patients were enrolled [22 women, 73.3%; median age 54 years (IQR 43-63) median cough duration 36 months (IQR 12-72)]. Clinically, an eosinophilic phenotype was identified in 11 patients, a chronic bronchitis phenotype in 15, and other phenotypes in 18, with frequent overlap. Airway inflammation or remodelling were present on histopathology in 27 of 30 patients (90%); a mixed inflammatory endotype predominated (15 patients), followed by eosinophilic (10), normal (3), and neutrophilic (2). Concordance between clinical phenotype and histopathological endotype was observed in 21 of 30 patients (70%). Subtle CT features of small-airway inflammation were found in 61.3% of patients but did not differ across endotypes. Conclusions: These findings demonstrate limited agreement between clinical phenotypes and tissue-level pathology in RCC, indicating that clinical phenotyping alone may be insufficient to capture its cellular and structural heterogeneity.

Cannabis use has increased greatly in the US since legalization occurred in many states, particularly by young adults ages 18-26. Recent survey data suggest that many young adults see smoking cannabis as carrying a low health risk, especially when compared to drinking alcohol or smoking tobacco. However, there is laboratory research and human health data suggesting that cannabis smoke has the potential to cause harm to users. A positive correlation between cannabis smoking and psychotic episodes has been established, as well as with respiratory symptoms such as chronic bronchitis. Research suggests that young adults are at particular risk for cognitive effects, and that cessation can improve health outcomes. Although, it is not possible to establish a definitive correlation between cannabis smoking and severe health outcomes such as cancer or other chronic diseases due to insufficient existing data and the technical limitations of the study designs. The gap in knowledge on cannabis health effects can be explained by various factors, including but not limited to insufficient quantities of clinical data, flawed study design, failure to account for the various methods of cannabis smoking, methods of cannabis use that do not involve smoking, dual use of tobacco or other substances by study participants, and an incomplete understanding of the pharmacology of cannabis and its non-psychoactive compounds. A complete knowledge of potential benefits of cannabis use is equally lacking; preliminary evidence suggests cannabis may possess anti-inflammatory properties, though these benefits have not yet been fully characterized or supported by sufficient clinical or basic research. While the Food and Drug Association (FDA) has approved the use of several cannabis-derived compounds such as cannabidiol (CBD) to treat select medical conditions, the use of cannabis itself has not received regulatory approval for treating any medical conditions. Due to the incomplete knowledge of any potential health effects of cannabis use, caution is advised to those considering the use of cannabis, particularly young adults.

Chronic pulmonary diseases, including cystic fibrosis, chronic obstructive pulmonary disease, and chronic bronchitis, as well as ventilator-associated pneumonia, are characterized by persistent infection of mucus-laden airways. Pseudomonas aeruginosa (PA) is a dominant pathogen in these conditions and produces volatile organic compounds (VOCs) that have been proposed as biomarkers of disease exacerbation; however, their immunopathogenic roles remain unclear. We investigated PA-derived VOCs using human bronchial epithelial air-liquid interface cultures and murine models. VOCs exposure significantly increased airway mucin expression and induced a proinflammatory response characterized by M1 macrophage polarization (iNOS[+]), neutrophil recruitment, and expansion of IL-17A-producing Thy1.2[+] lymphocytes. Functional depletion of macrophages, neutrophils, or IL-17A in vivo each attenuated mucin production and goblet cell metaplasia, indicating non-redundant contributions to mucus pathology. In vitro, IL-17A neutralization partially restored FOXA2 expression and reduced mucin production, supporting a role in mucus regulation. On the mechanistic level, we discovered an IL-17A-dependent dual-axis pathway involving both epithelial cell-mediated autocrine and lymphocyte-mediated paracrine signaling that contributes to the feed-forward loop of inflammation and enhances the signaling pathways regulating mucus hypersecretion in airways. We conclude that PA VOCs activate multiple proinflammatory responses to convergently drive mucus pathogenesis in the diseased lung.