Changes of histamine receptors and CC chemokines in nasal epithelial cells and fibroblasts after respiratory syncytial virus infection.

BACKGROUND: Respiratory syncytial virus (RSV) is reported as the most influential factor that triggers hyperreactivity of the airway and causes asthma in infants and children. However, the mechanisms remain to be elucidated. The study evaluated the changes in the levels of four types of histamine receptor (HR) and CC chemokines, such as eotaxin and regulated on activation, normal T cell expressed and presumably secreted (RANTES), in nasal epithelial cells and fibroblasts after RSV infection.

METHODS: Nasal cavity mucosa attained from 20 patients who had undergone inferior turbinoplasty were cleaned by normal saline mixed with gentamicin. Each sample was divided in half. One-half was used for incubation of epithelial cells, and the other half was used for culturing fibroblasts. The levels of HR 1 (H1R), 2 (H2R), 3 (H3R), 4 (H4R), eotaxin, and RANTES were measured by real-time polymerase chain reaction 0, 12, and 36 hours after infection with RSV.

RESULTS: H1R was significantly increased at 12 and 36 hours compared with 0 hours in both cell types. The level of H2R was significantly increased in epithelial cells from 0 to 36 and 12 to 36 hours and in fibroblasts from 0 to 12 and 0 to 36 hours. There were significant increases of H3R level in fibroblasts from 0 to 12 and 0 to 36 hours, and of H4R in epithelial cells and fibroblasts from 0 to 12 and 0 to 36 hours. Eotaxin and RANTES were also significantly increased in both epithelial cells and fibroblasts from 0 to 12 and 0 to 36 hours.

CONCLUSION: RSV infection increases the levels of all four HRs, especially H1R and H2R, as well as the levels of eotaxin and RANTES in nasal epithelial cells and fibroblasts. These findings suggest that RSV infection might cause respiratory tract hyperreactivity by increasing the content of HRs and CC chemokines.