ArticleRespiratory research2017
The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL).
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Trial
- Dual inhibition of intercellular adhesion molecule-1 and nucleolin reduces RSV infection efficiency in human respiratory organoids.Molecular therapy. Nucleic acids · 2026Article
- Low-Dose Radiation Sensitizes Human Nasal Epithelium to Viral Inflammation despite Preserved Structural Integrity.International archives of allergy and immunology · 2026Article
- Article
- Rhinovirus C15 infection induces airway epithelial cell remodeling and robust inflammatory responses: Potential implications for airway obstruction in children.Mucosal immunology · 2025Article
- Clinical Significance of Rhinoviruses and Progress Toward Vaccination.Allergy, asthma & immunology research · 2025Review
- Circulating biomarkers of airflow limitation across the life span.The Journal of allergy and clinical immunology · 2024Article
- Platelet Activating Factor Receptor and Intercellular Adhesion Molecule-1 Expression Increases in the Small Airway Epithelium and Parenchyma of Patients with Idiopathic Pulmonary Fibrosis: Implications for Microbial Pathogenesis.Journal of clinical medicine · 2024Article
- Review
- Can the ADO Index Be Used as a Predictor of Mortality from COVID-19 in Patients with COPD?International journal of chronic obstructive pulmonary disease · 2024Observational
- Determinants of immunoglobulin G responses to respiratory syncytial virus and rhinovirus in children and adults.Frontiers in immunology · 2024Article
- In-silico identification and prioritization of therapeutic targets of asthma.Scientific reports · 2023Article
- Oxidative Stress and Lung Fibrosis: Towards an Adverse Outcome Pathway.International journal of molecular sciences · 2023Review
- Non-typeableEuropean respiratory review : an official journal of the European Respiratory Society · 2022Review
- Increased SARS-CoV-2 Infection, Protease, and Inflammatory Responses in Chronic Obstructive Pulmonary Disease Primary Bronchial Epithelial Cells Defined with Single-Cell RNA Sequencing.American journal of respiratory and critical care medicine · 2022Article
- Susceptibility of Patients with Airway Disease to SARS-CoV-2 Infection.American journal of respiratory and critical care medicine · 2022Article
- Targeting intercellular adhesion molecule-1 (ICAM-1) to reduce rhinovirus-induced acute exacerbations in chronic respiratory diseases.Inflammopharmacology · 2022Review
- Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Chronic obstructive pulmonary disease and COVID-19: interrelationships.Current opinion in pulmonary medicine · 2022Review
- Mechanisms, Pathophysiology and Currently Proposed Treatments of Chronic Obstructive Pulmonary Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundICAM-1 is a major receptor for ~60% of human rhinoviruses, and non-typeable Haemophilus influenzae, two major pathogens in COPD. Increased cell-surface expression of ICAM-1 in response to tobacco smoke exposure has been suggested. We have investigated epithelial ICAM-1 expression in both the large and small airways, and lung parenchyma in smoking-related chronic airflow limitation (CAL) patients.
methodsWe evaluated epithelial ICAM-1 expression in resected lung tissue: 8 smokers with normal spirometry (NLFS); 29 CAL patients (10 small-airway disease; 9 COPD-smokers; 10 COPD ex-smokers); Controls (NC): 15 normal airway/lung tissues. Immunostaining with anti-ICAM-1 monoclonal antibody was quantified with computerized image analysis. The percent and type of cells expressing ICAM-1 in large and small airway epithelium and parenchyma were enumerated, plus percentage of epithelial goblet and submucosal glands positive for ICAM- 1.
resultsA major increase in ICAM-1 expression in epithelial cells was found in both large (p < 0.006) and small airways (p < 0.004) of CAL subjects compared to NC, with NLFS being intermediate. In the CAL group, both basal and luminal areas stained heavily for ICAM-1, so did goblet cells and sub-mucosal glands, however in either NC or NLFS subjects, only epithelial cell luminal surfaces stained. ICAM-1 expression on alveolar pneumocytes (mainly type II) was slightly increased in CAL and NLFS (p < 0.01). Pack-years of smoking correlated with ICAM-1 expression (r = 0.49; p < 0.03).
conclusionAirway ICAM-1 expression is markedly upregulated in CAL group, which could be crucial in rhinoviral and NTHi infections. The parenchymal ICAM-1 is affected by smoking, with no further enhancement in CAL subjects.
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