title: Leptin Is Oversecreted by Respiratory Syncytial Virus-Infected Bronchial Epithelial Cells and Regulates Th2 and Th17 Cell Differentiation.
abstract: BACKGROUND
  Infection of human bronchial epithelial cells (hBECs) with respiratory syncytial virus (RSV) has been shown to induce a Th lymphocyte subset drift, e.g. enhanced differentiation of Th2 and Th17 subsets, which is a classic characteristic of asthma. However, the molecules responsible for the drift in Th subsets remain unknown. This study aims to determine the expression of leptin in RSV-infected hBECs, and its role in Th2 and Th17 cell differentiation and extracellular regulated kinase (ERK) 1/2 phosphorylation.
  
  
  METHODS
  Cultured hBECs were infected with RSV. mRNA expression of the LEP gene in cells was measured by real-time PCR while LEP protein secretion in culture medium was measured by ELISA. Th differentiation was investigated in cultured human peripheral blood mononuclear cells following stimulation with recombinant human leptin. Th2 and Th17 subsets were examined by flow cytometry. Phosphorylation of the ERK1/2 protein in lymphocytes was detected by Western blot and immunofluorescence.
  
  
  RESULTS
  LEP mRNA expression was significantly upregulated in RSV-infected hBECs while the leptin protein level in the supernatants of RSV-infected hBECs was significantly increased. Stimulation of lymphocytes with leptin increased the differentiation of the Th17 subset and ERK1/2 phosphorylation, but suppressed Th2 subset differentiation.
  
  
  CONCLUSIONS
  Leptin was oversecreted by RSV-infected hBECs, which promoted Th17 subset differentiation but suppressed Th2 subset differentiation possibly via regulating ERK1/2 phosphorylation.
authors.affiliation: Department of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Xiangya Hospital, Changsha, PR China.
authors.forename: Ling
authors.initials: L
authors.lastname: Qin
authors.forename: Yu-rong
authors.initials: YR
authors.lastname: Tan
authors.forename: Cheng-ping
authors.initials: CP
authors.lastname: Hu
authors.forename: Xiao-ai
authors.initials: XA
authors.lastname: Liu
authors.forename: Ruo-xi
authors.initials: RX
authors.lastname: He
mesh_terms: D001249:Asthma / Q000276:immunology / Q000821:virology*; D002454:Cell Differentiation / Q000276:immunology; D002460:Cell Line; D004847:Epithelial Cells / Q000378:metabolism / Q000821:virology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D020738:Leptin / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D012333:RNA, Messenger / Q000096:biosynthesis; D020545:Respiratory Mucosa / Q000166:cytology / Q000378:metabolism / Q000821:virology*; D018357:Respiratory Syncytial Virus Infections / Q000473:pathology*; D018113:Respiratory Syncytial Virus, Human / Q000472:pathogenicity*; D058504:Th17 Cells / Q000166:cytology / Q000276:immunology; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology
chemical_list: D020738:Leptin; D012333:RNA, Messenger; D048049:Extracellular Signal-Regulated MAP Kinases