Expression of intercellular adhesion molecule-1 (ICAM-1) in nasal epithelial cells of atopic subjects: a mechanism for increased rhinovirus infection?

Authors

  • A. Bianco,

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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  • S. C. Whiteman,

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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  • S. K. Sethi,

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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  • J. T. Allen,

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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  • R. A. Knight,

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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  • M. A. Spiteri

    1. Lung Injury and Inflammation Research Group, Centre for Cell and Molecular Medicine, Keele University, and Department of Respiratory Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK
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Correspondence: Dr Monica A. Spiteri, Department of Respiratory Medicine, North Staffordshire Hospital Trust, Newcastle Road, Stoke-on-Trent, Staffordshire ST4 6QG, UK.E-mail: m.spiteri@virgin.net

Abstract

Since clinical experimental studies indicate that upper respiratory tract viral infections may exacerbate acute asthma symptoms in atopic/asthmatic individuals, we have investigated the expression and modulation of ICAM-1 on human nasal epithelial cells (HNEC) from normal and atopic subjects. ICAM-1 is the attachment molecule for the majority of serotypes of human rhinovirus (HRV), including HRV-14, and is also critical for the migration and activation of immune effector cells. Basal ICAM-1 expression was significantly higher in HNEC obtained by brushings from atopic compared with non-atopic subjects (P = 0·031), and was also significantly increased on atopic HNEC harvested in season compared with out of season (P < 0·05). Atopic HNEC showed further up-regulation in ICAM-1 expression when cultured with clinically relevant allergen (P = 0·032). ICAM-1 levels on normal HNEC were also increased by infection with HRV-14 (P < 0·05). Basal expression of ICAM-1 on atopic nasal polyp epithelial cells (EC) was significantly higher than on both normal and atopic nasal HNEC. This elevated nasal polyp ICAM-1 level was not increased further by allergen, although HRV infection resulted in a small significant increase. Recovered viral titres from HRV-infected nasal polyp EC were 1·5-fold higher than from infected normal nasal HNEC. The data are consistent with the hypothesis that allergen, by enhancing expression of the HRV attachment target on host cells, facilitates viral infection in atopic subjects; simultaneously HRV-induced increases in ICAM-1 levels would favour migration and activation of immune effector cells to the airway, resulting in enhanced atopic inflammation.

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