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.
Highlights
intercellular adhesion molecule 1 (ICAM-1) is a major receptor for ~60% of human rhinoviruses, and non-typeable Haemophilus influenzae, two major pathogens in Chronic obstructive pulmonary disease (COPD)
ICAM-1 expression in epithelium of large and small airways Compared to normal controls, epithelial staining was increased in the apical areas in the NLFS group, whereas in the chronic airflow limitation (CAL) group, heavy ICAM-1 expression was observed throughout the airway epithelium, including both the apical and basal cells, though basal cell staining was heaviest (Figs. 1 and 2)
ICAM-1 positive cells in the airway reticular basement membrane (Rbm) The Rbm in smokers and especially in COPD have been reported as hyper-cellular [24], and this was true in this study
Summary
ICAM-1 is a major receptor for ~60% of human rhinoviruses, and non-typeable Haemophilus influenzae, two major pathogens in COPD. 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. Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality worldwide. It is a disabling condition resulting from damage inflicted by noxious particles and gases, mainly from cigarette smoke leading to airway remodeling and poorly-reversible airflow obstruction [1]. COPD patients are often prone to episodes of COPD is seriously complicated by bacterial and viral infections. Viral infections are associated with more severe exacerbations [4]. Human rhinoviruses (HRVs) make up approximately 50% of all viruses isolated from COPD patients [5].
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