Modulation of the epithelial inflammatory response to rhinovirus in an atopic environment.
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-beta1 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-beta1 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.
Xatzipsalti
M
M
Allergy Department, 2nd Pediatric Clinic, University of Athens, Athens, Greece. marax5873@hotmailco.uk
Psarros
F
F
Konstantinou
G
G
Gaga
M
M
Gourgiotis
D
D
Saxoni-Papageorgiou
P
P
Papadopoulos
N G
NG
D000328:Adult; D000917:Antibody Formation; D001249:Asthma / Q000097:blood* / Q000209:etiology; D001980:Bronchi / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001991:Bronchitis / Q000378:metabolism* / Q000473:pathology / Q000821:virology*; D016923:Cell Death; D002478:Cells, Cultured; D017077:Culture Media, Conditioned / Q000494:pharmacology; D016207:Cytokines / Q000096:biosynthesis; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000150:complications / Q000276:immunology; D018836:Inflammation Mediators / Q000378:metabolism*; D007371:Interferon-gamma / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism*; D010850:Picornaviridae Infections / Q000378:metabolism* / Q000503:physiopathology; D012229:Rhinovirus / Q000254:growth & development; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D015854:Up-Regulation; D014779:Virus Replication / Q000187:drug effects
D017077:Culture Media, Conditioned; D016207:Cytokines; D018836:Inflammation Mediators; D053773:Transforming Growth Factor beta1; D007371:Interferon-gamma