Shukla, SD and Mahmood, MQ and Weston, S and Latham, R and Muller, HK and Sohal, SS and Walters, EH, The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL), Respiratory research, 18 pp. 1-10. ISSN 1465-9921 (2017) [Refereed Article]
Copyright 2017 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/
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 < 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,/i> = 0.49; p < 0.03).
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:||Refereed Article|
|Keywords:||COPD, ICS, inflammation, infections|
|Research Division:||Biomedical and Clinical Sciences|
|Research Group:||Cardiovascular medicine and haematology|
|Research Field:||Respiratory diseases|
|Objective Group:||Clinical health|
|Objective Field:||Clinical health not elsewhere classified|
|UTAS Author:||Shukla, SD (Mr Shakti Shukla)|
|UTAS Author:||Mahmood, MQ (Mr Malik Mahmood)|
|UTAS Author:||Weston, S (Mr Steven Weston)|
|UTAS Author:||Latham, R (Mr Roger Latham)|
|UTAS Author:||Muller, HK (Professor Konrad Muller)|
|UTAS Author:||Sohal, SS (Dr Sukhwinder Sohal)|
|UTAS Author:||Walters, EH (Professor Haydn Walters)|
|Web of Science® Times Cited:||29|
|Deposited By:||Health Sciences|
|Downloads:||114 View Download Statistics|
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