期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 110, 期 5, 页码 752-756出版社
MOSBY, INC
DOI: 10.1067/mai.2002.128581
关键词
Permeability; transendothelial electrical resistance; rhinovirus; eosinophils; transmigration; asthma; cytokines; adhesion
资金
- NHLBI NIH HHS [HL-60993] Funding Source: Medline
Background: Rhinovirus (RV) infections can result in asthma exacerbations in both adults and children. Respiratory epithelium, the primary site of RV replication, responds to the viral infection by generating a variety of cytokines and chemokines capable of promoting airway inflammation and hence might increase asthma severity. Some of these mediators might also affect the permeability of underlying vascular endothelium. Objective: We hypothesized that RV infections can promote airway inflammation and thus asthma by enhancing local vascular permeability. Methods: Confluent human lung microvascular endothelial cell (HMVEC-L) monolayers were used as an in vitro model of vascular endothelium to determine whether cytokines associated with RV-induced infections are capable of modulating endothelial cell permeability as measured by means of transendothelial electrical resistance. Recombinant cytokines and chemokines were added to confluent HMVEC-L monolayers cultured on Transwell filters, and permeability was measured as decreased electrical resistance over time. Eosinophil transendothelial migration was assessed under the same experimental conditions. Results: TNF-alpha, IL-1beta, and IFN-gamma significantly increased HMVEC-L permeability. In contrast, GM-CSF, G-CSF, IL-8, IL-6, and RANTES had no effect. Although incubation of HMVEC-L monolayers with either TNF-alpha. or IL-1beta promoted eosinophil migration, IFN-gamma had no effect, indicating that enhanced permeability alone was not sufficient for eosinophil infiltration. Conclusion: Select cytokines, generated in response to RV infection, can increase vascular permeability and might provide a mechanism by which RV infection can lead to edema, cellular infiltration, and inflammation and thus compromised airflow.
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