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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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Shukla, SD, Mahmood, MQ ORCID: 0000-0003-1333-7940, Weston, S, Latham, R ORCID: 0000-0002-6621-1949, Muller, HK, Sohal, SS ORCID: 0000-0001-9627-6498 and Walters, EH ORCID: 0000-0002-0993-4374 2017 , 'The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL)' , Respiratory research, vol. 18 , pp. 1-10 , doi: 10.1186/s12931-016-0483-8.

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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
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)

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