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Modulation of the epithelial inflammatory response to rhinovirus in an atopic environment
Author(s) -
Xatzipsalti M.,
Psarros F.,
Konstantinou G.,
Gaga M.,
Gourgiotis D.,
SaxoniPapageorgiou P.,
Papadopoulos N. G.
Publication year - 2008
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2007.02906.x
Subject(s) - rhinovirus , immunology , peripheral blood mononuclear cell , immune system , asthma , respiratory system , inflammation , cytotoxicity , respiratory epithelium , epithelium , medicine , biology , virus , in vitro , pathology , biochemistry
Summary 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.