PT - JOURNAL ARTICLE AU - Emily J. Swindle AU - Cornelia Blume AU - Peter Collins AU - Dean D. Metcalfe AU - Stephen T. Holgate AU - Donna E. Davies TI - LSC 2013 abstract - Mast cells support rhinovirus but not respiratory syncytial virus replication and contribute to the pro-inflammatory response to rhinovirus DP - 2013 Sep 01 TA - European Respiratory Journal PG - PP140 VI - 42 IP - Suppl 57 4099 - http://erj.ersjournals.com/content/42/Suppl_57/PP140.short 4100 - http://erj.ersjournals.com/content/42/Suppl_57/PP140.full SO - Eur Respir J2013 Sep 01; 42 AB - Rationale: Respiratory virus infections (Respiratory Syncytial Virus (RSV), Rhinovirus (RV)) are major causes of persistent wheeze in infants and predict the development of asthma in later life. Mast cell (MC) numbers and reticular basement membrane thickness are increased in children with recurrent wheeze at age 1yr and predicts respiratory morbidity at age 3yrs. This suggests an important interaction between viral infection and MCs leading to allergic inflammation and development of asthma in young children. Since MCs have a key role in innate immunity to pathogens we hypothesized that MCs contribute to the innate immune response to viral infection in asthma.Methods: The human MC line, LAD2, was infected with RSV or RV16 for 1h. After washing, MCs were cultured for 24h. Viral infection was determined by detection of gfp-RSV by flow cytometry or RV viral RNA by real-time PCR and virion release by TCID50 assay. Anti-viral and pro-inflammatory responses were assessed by real-time PCR. Degranulation was assessed by β-hex release.Results: Exposure of MCs to RV16 but not RSV resulted in detectable viral RNA and increased IFNβ expression indicating that MCs support RV replication and mount an antiviral response. Virions were also released by MCs exposed to RV demonstrating that MCs release infective virus particles. RSV and RV16 did not induce MC degranulation. Investigations of mediator release by MCs showed increased IP-10 but not IL-8 or RANTES gene expression in response to RV16.Conclusion: MCs contribute to the pro-inflammatory response to RV16 and may act as a viral reservoir and contribute to the development of asthma in early life.