title: Chemokine-like factor 1, a novel cytokine, contributes to airway damage, remodeling and pulmonary fibrosis.
abstract: BACKGROUND
  Chemokine-like factor 1 (CKLF1) was recently identified as a novel cytokine. The full-length CKLF1 cDNA contains 530 bp encoding 99 amino acid residues with a CC motif similar to that of other CC family chemokines. Recombinant CKLF1 exhibits chemotactic activity on leucocytes and stimulates proliferation of murine skeletal muscle cells. We questioned whether CKLF1 could be involved in the pathogenesis of inflammation and proliferation in the lung. Therefore we used efficient in vivo gene delivery method to investigate the biological effect of CKLF1 in the murine lung.
  
  
  METHODS
  CKLF1-expressing plasmid, pCDI-CKLF1, was constructed and injected into the skeletal muscles followed by electroporation. Lung tissues were obtained at the end of week 1, 2, 3 and 4 respectively after injection. The pathological changes in the lungs were observed by light microscope.
  
  
  RESULTS
  A single intramuscular injection of CKLF1 plasmid DNA into BALB/c mice caused dramatic pathological changes in the lungs of treated mice. These changes included peribronchial leukocyte infiltration, epithelial shedding, collagen deposition, proliferation of bronchial smooth muscle cells and fibrosis of the lung.
  
  
  CONCLUSIONS
  The sustained morphological abnormalities of the bronchial and bronchiolar wall, the acute pneumonitis and interstitial pulmonary fibrosis induced by CKLF1 were similar to phenomena observed in chronic persistent asthma, acute respiratory distress syndrome and severe acute respiratory syndrome. These data suggest that CKLF1 may play an important role in the pathogenesis of these important diseases and the study also implies that gene electro-transfer in vivo could serve as a valuable approach for evaluating the function of a novel gene in animals.
authors.affiliation: Department of Respiratory Diseases, First Affiliated Hospital, Peking University, Beijing 100034, China.
authors.forename: Ya-xia
authors.initials: YX
authors.lastname: Tan
authors.forename: Wen-ling
authors.initials: WL
authors.lastname: Han
authors.forename: Ying-yu
authors.initials: YY
authors.lastname: Chen
authors.forename: Neng-tai
authors.initials: NT
authors.lastname: Ouyang
authors.forename: Yan
authors.initials: Y
authors.lastname: Tang
authors.forename: Feng
authors.initials: F
authors.lastname: Li
authors.forename: Pei-guo
authors.initials: PG
authors.lastname: Ding
authors.forename: Xiao-lan
authors.initials: XL
authors.lastname: Ren
authors.forename: Guang-qiao
authors.initials: GQ
authors.lastname: Zeng
authors.forename: Jing
authors.initials: J
authors.lastname: Ding
authors.forename: Tong
authors.initials: T
authors.lastname: Zhu
authors.forename: Da-long
authors.initials: DL
authors.lastname: Ma
authors.forename: Nan-shan
authors.initials: NS
authors.lastname: Zhong
mesh_terms: D000818:Animals; D001483:Base Sequence; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002465:Cell Movement; D018925:Chemokines / Q000235:genetics / Q000502:physiology*; D018274:Electroporation; D006801:Humans; D008168:Lung / Q000473:pathology*; D062792:MARVEL Domain-Containing Proteins; D051379:Mice; D008807:Mice, Inbred BALB C; D008969:Molecular Sequence Data; D010957:Plasmids; D011658:Pulmonary Fibrosis / Q000209:etiology*
chemical_list: C432676:CKLF protein, human; D018925:Chemokines; D062792:MARVEL Domain-Containing Proteins