RT Journal Article
SR Electronic
T1 Rhinovirus respiratory adhesion sites are upregulated in smokers and chronic airflow limitation (CAL)
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP PA2613
DO 10.1183/13993003.congress-2016.PA2613
VO 48
IS suppl 60
A1 Shakti Shukla
A1 Malik Mahmood
A1 Konrad Muller
A1 Steven Weston
A1 Sukhwinder Sohal
A1 Haydn Walters
YR 2016
UL http://erj.ersjournals.com/content/48/suppl_60/PA2613.abstract
AB Introduction: ICAM-1 is a receptor for 90% of human rhinoviruses, and non-typeable Haemophilus influenzae, two major pathogens in COPD.Aims: We have investigated epithelial ICAM-1 expression in airways and alveoli in relation to smoking and CAL.Methods: We evaluated epithelial ICAM-1 expression in both large and small airways from resected tissue: 8 smokers with normal spirometry; 28 CAL patients (10 small airway dysfunction; 8 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 alveolar type I and type II pneumocytes 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. The staining patterns were quite intriguing: in the CAL group both basal and luminal areas stained heavily for ICAM-1, but so did goblet cells and sub-mucosal glands. These features were not evident in either NC or NLFS subjects, with 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 smoking correlated with ICAM-1 expression (r=0.49; p<0.03).Conclusion: Airway ICAM-1 expression is especially marked in the CAL group, which could be crucial in viral infection and secondary bacterial infections. The lung parenchyma ICAM-1 is less affected and only by smoking.