期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 121, 期 5, 页码 1155-1160出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2008.02.009
关键词
B7 homologs; costimulatory ligands; cell-surface molecules; human airway epithelial cells; rhinovirus infection; double-stranded RNA
资金
- NCRR NIH HHS [M01-RR-02719, M01 RR002719] Funding Source: Medline
- NHLBI NIH HHS [R01 HL078860-02, HL078860, R37 HL068546, HL068546, R01 HL078860, R01 HL068546] Funding Source: Medline
- NIAID NIH HHS [AI57400, K23 AI057400] Funding Source: Medline
Background: T-cell infiltration of the epithelium is a key feature of chronic rhinosinusitis and asthma. Viral infections are an important cause of disease exacerbations. We have found virus-induced expression of T cell-interacting ligands, B7 homolog costimulatory molecules, on airway epithelium. Objective: We tested the ability of human rhinovirus (HRV) 16 and double-stranded RNA (dsRNA) to alter the expression of B7 homologs on human airway epithelial cells. Methods: BEAS2B and primary human airway epithelial cells were exposed in vitro to dsRNA (25 mu g/mL) or HRV-16, and then expression of cell-surface protein and mRNA for B7 homologs was assessed by means of flow cytometry and real-time PCR, respectively. Additionally, human subjects were infected with HRV-16 in vivo, and mRNA for B7 homologs was assessed by means of real-time PCR in fresh nasal epithelial cell scrapings obtained before and daily up to 4 days after infection. Results: dsRNA exposure of BEAS2B and human primary bronchial epithelial cells resulted in increased levels of cell-surface and mRNA expression of B7-H1 and B7-DC but not B7-H2 or B7-H3. Exposure of primary cells to HRV-16 resulted in induction of cell-surface expression of B7-H1 and B7-DC. Pretreatment with fluticasone propionate failed to suppress the induction of B7-H1 and B7-DC. Nasal scrapings taken at the time of peak symptom scores (3 days) after infection of 6 human subjects with HRV-16 displayed selective induction of levels of mRNA for B7-H1 and B7-DC. Conclusion: These data show that HRV-16 infection or exposure to dsRNA induces epithelial B7-H1 and B7-DC.
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