the changes of th17/treg and related cytokines: il-17, il-23, il-10, and tgf-β in respiratory syncytial virus bronchiolitis rat model

Respiratory syncytial virus (rsv) is the leading cause of bronchiolitis and hospitalization that lead to high morbidity and mortality among young infants. t helper 17 (th17) cells and regulatory t cells (tregs) play essential roles in the pathogenesis of autoimmune, cancer, and inflammatory diseases. however, whether changes in tcell subsets are related to the systemic immune responses in rsvcaused bronchiolitis merit further investigation. threeweekold sprague dawley (sd) rats were randomly divided into the normal control (nc) and rsv bronchiolitis (rsvb) groups. an rsvb model was successfully established using nasal drip containing rsv. furthermore, pathological changes in the lung tissues were observed using hematoxylin and eosin staining. flow cytometry determined the levels of th17 and treg subsets. the related cytokines were measured using enzymelinked immunosorbent assay (elisa). the expression levels of related transcription factors, such as rorγt and foxp3, were examined using realtime quantitative pcr and western blot analysis. the rsvb group exhibited pulmonary interstitial hyperemia and edema, inflammatory cell infiltration, wide alveolar septa, and bronchial collapse and deformation. the percentage of th17 cells in rsvb group was about 2.3 fold higher than that of nc group, and the concentration of il17, il23 and rorγt was higher than in nc group. in contrast, the percentage of treg cells in the rsvb group was approximately 0.7 fold lower than that in the nc group, and the levels of il10, tgfβ, and foxp3 in the rsvb group were lower than those in the nc group. the above results were statistically significant. the changes of th17/treg, and their associated cytokines, specific transcription factors, are present in rsv bronchiolitis model rats, which may play an important role in the pathogenesis of rsv bronchiolitis.