The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL).

Shukla, SD; Mahmood, MQ; Weston, S; Latham, R; Muller, HK; Sohal, SS; Walters, EH

The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL).

Shukla, SD Mahmood, MQ Weston, S Latham, R Muller, HK Sohal, SS Walters, EH

Permalink

Publisher:: BMC
Publication Type:: Journal Article
Citation:: Respir Res, 2017, 18, (1), pp. 6
Issue Date:: 2017-01-05

Open Access

Copyright Clearance Process

Recently Added
In Progress
Open Access

This item is open access.

Adobe PDF

Download Published versionAdobe PDF (1.59 MB)

View on publisher's site

View statistics

Full metadata record

Field	Value	Language
dc.contributor.author	Shukla, SD
dc.contributor.author	Mahmood, MQ
dc.contributor.author	Weston, S
dc.contributor.author	Latham, R
dc.contributor.author	Muller, HK
dc.contributor.author	Sohal, SS
dc.contributor.author	Walters, EH
dc.date.accessioned	2022-10-04T21:04:12Z
dc.date.available	2016-12-06
dc.date.available	2022-10-04T21:04:12Z
dc.date.issued	2017-01-05
dc.identifier.citation	Respir Res, 2017, 18, (1), pp. 6
dc.identifier.issn	1465-9921
dc.identifier.issn	1465-993X
dc.identifier.uri	http://hdl.handle.net/10453/162303
dc.description.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 < 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). 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.
dc.format	Electronic
dc.language	eng
dc.publisher	BMC
dc.relation.ispartof	Respir Res
dc.relation.isbasedon	10.1186/s12931-016-0483-8
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1102 Cardiorespiratory Medicine and Haematology, 1103 Clinical Sciences
dc.subject.classification	Respiratory System
dc.subject.mesh	Adult
dc.subject.mesh	Aged
dc.subject.mesh	Female
dc.subject.mesh	Humans
dc.subject.mesh	Intercellular Adhesion Molecule-1
dc.subject.mesh	Male
dc.subject.mesh	Middle Aged
dc.subject.mesh	Picornaviridae Infections
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Respiratory Mucosa
dc.subject.mesh	Rhinovirus
dc.subject.mesh	Smoking
dc.subject.mesh	Up-Regulation
dc.subject.mesh	Respiratory Mucosa
dc.subject.mesh	Humans
dc.subject.mesh	Rhinovirus
dc.subject.mesh	Picornaviridae Infections
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Intercellular Adhesion Molecule-1
dc.subject.mesh	Smoking
dc.subject.mesh	Up-Regulation
dc.subject.mesh	Adult
dc.subject.mesh	Aged
dc.subject.mesh	Middle Aged
dc.subject.mesh	Female
dc.subject.mesh	Male
dc.title	The main rhinovirus respiratory tract adhesion site (ICAM-1) is upregulated in smokers and patients with chronic airflow limitation (CAL).
dc.type	Journal Article
utslib.citation.volume	18
utslib.location.activity	England
utslib.for	1102 Cardiorespiratory Medicine and Haematology
utslib.for	1103 Clinical Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Health
utslib.copyright.status	open_access	*
dc.date.updated	2022-10-04T21:04:08Z
pubs.issue	1
pubs.publication-status	Published online
pubs.volume	18
utslib.citation.issue	1

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 < 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). 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.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/162303