Modulation of the epithelial inflammatory response to rhinovirus in an atopic environment
Article first published online: 30 DEC 2007
© 2007 The Authors
Clinical & Experimental Allergy
Volume 38, Issue 3, pages 466–472, March 2008
How to Cite
Xatzipsalti, M., Psarros, F., Konstantinou, G., Gaga, M., Gourgiotis, D., Saxoni-Papageorgiou, P. and Papadopoulos, N. G. (2008), Modulation of the epithelial inflammatory response to rhinovirus in an atopic environment. Clinical & Experimental Allergy, 38: 466–472. doi: 10.1111/j.1365-2222.2007.02906.x
- Issue published online: 30 DEC 2007
- Article first published online: 30 DEC 2007
- Submitted 5 February 2007; revised 19 September 2007; accepted 2 November 2007
- immune response;
Background Immune responses to rhinovirus (RV) as well as direct effects of RV on respiratory epithelium may contribute to the induction of asthma exacerbations.
Objective To evaluate the effect of the environment resulting from an atopic immune response on RV-induced epithelial inflammation, replication and cytotoxicity.
Methods Peripheral blood mononuclear cells (PBMC) from atopic asthmatic subjects and matched controls (12 pairs) were isolated and stimulated by RVs. Human bronchial epithelial (BEAS-2B) cells were infected with RV in the presence of conditioned media from RV-stimulated PBMC cultures. IL-6, IL-8, RANTES and TGF-β1 levels were measured by ELISA, RV-induced cytotoxicity by a colorimetric method and RV titres on Ohio-HeLa cells.
Results RV-induced epithelial production of IL-6, IL-8 and RANTES was significantly lower, while TGF-β1 was higher when cells were exposed to conditioned media from atopic asthmatic subjects compared with those from normal controls. Exposure to the ‘atopic’ environment also resulted in elevated RV titres and increased RV-induced cytotoxicity.
Conclusions Under the influence of an atopic environment, the epithelial inflammatory response to RV is down-regulated, associated with increased viral proliferation and augmented cell damage, while TGF is up-regulated. These changes may help explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections and indicate a mechanism through which viral infections may promote airway remodelling.