title: [Th17/Treg imbalance mediated by IL-8 in RSV-infected bronchial epithelial cells].
abstract: OBJECTIVE
  To explore the mechanisms for an increase in susceptibility of asthma induced by respiratory syncytial virus (RSV), to observe the expression of interleukin-8 (IL-8) in human bronchial epithelial cells (HBECs) after RSV infection and to invesigate the regulatory effect of IL-8 on Th17/Treg differentiation.
  
  
  METHODS
  HBECs were divided into a control group and a RSV infected group. The RSVE-infected model of HBECs was established and examined. The expression of IL-8 mRNA was detected by real-time PCR, and the levels of IL-8 were measured by ELISA. Peripheral blood lymphocytes in healthy people were extracted and divided into a control group and an IL-8 treatment group. Based on concentration of IL-8 in RSV-infected HBECs, lymphocytes were treated by a matched concentration of human recombinant IL-8 for 24 h. The distribution of Th17 and Treg subsets in lymphocytes were examined by flow cytometry.
  
  
  RESULTS
  The RSV-infected HBECs model was successfully established. The infected HBECs were still able to split and passage. The RSV could be detected in every passage in the infected cells. Virus particles indicated by bright yellow green fluorescence were seen under fluorescence microscope. Edema of mitochondrias, expansion of endoplasmic reticulum, fissure around nucleus and intracellular virus particles were all observed under electron microscope. The expression IL-8 mRNA were significantly enhanced in the RSV-infected group, and the level of IL-8 in the RSV-infected group was higher than that in the control group (P<0.05). After IL-8 treatment for 24 h, the ratio of Th17 subsets in lymphocytes were dramatically increased compared to the control group (P<0.05), but there was no difference in the ratio of Treg subsets between the 2 groups (P>0.05).
  
  
  CONCLUSIONS
  Over-secretion of IL-8 by the RSV-infected HBECs may promote the differentiation of Th17 subsets and maintain the Th17/Tred imbalance.
authors.affiliation: Department of Respiratory, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Qin
authors.affiliation: Department of Respiratory, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Juntao
authors.initials: J
authors.lastname: Feng
authors.affiliation: Department of Respiratory, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Chengping
authors.initials: C
authors.lastname: Hu
authors.affiliation: Department of Respiratory, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Respiratory, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Ruichao
authors.initials: R
authors.lastname: Niu
mesh_terms: D002454:Cell Differentiation; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000187:drug effects* / Q000821:virology; D005434:Flow Cytometry; D006801:Humans; D016209:Interleukin-8 / Q000276:immunology* / Q000494:pharmacology; D060888:Real-Time Polymerase Chain Reaction; D011994:Recombinant Proteins / Q000494:pharmacology; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology*; D012136:Respiratory Syncytial Viruses; D050378:T-Lymphocytes, Regulatory / Q000166:cytology*; D058504:Th17 Cells / Q000166:cytology*
chemical_list: C508606:CXCL8 protein, human; D016209:Interleukin-8; D011994:Recombinant Proteins