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The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL)
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Abstract
Background:ICAM-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.Methods: We 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.Results: A major increase in ICAM-1 expression in epithelial cells was found in both large (p p p r,/i> = 0.49; p Conclusion: Airway 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.
Item Type: | Article |
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Authors/Creators: | Shukla, SD and Mahmood, MQ and Weston, S and Latham, R and Muller, HK and Sohal, SS and Walters, EH |
Keywords: | COPD, ICS, inflammation, infections |
Journal or Publication Title: | Respiratory research |
Publisher: | Current Science Ltd. |
ISSN: | 1465-9921 |
DOI / ID Number: | 10.1186/s12931-016-0483-8 |
Copyright Information: | Copyright 2017 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/ |
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