title: The effect of human antibacterial peptide LL-37 in the pathogenesis of chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Previous research has shown that innate immune system was more important than the acquired immune system in the pathogenesis of COPD. LL-37 is the only human cathelicidin identified so far. As an integral part of the innate immune system, besides antibacterial activity, its chemotactic activity, damage repairing, influencing apoptosis and its cytotoxicity are attracting people's attention. The aim of the present study was to evaluate role of LL-37 in the pathogenesis of COPD.
  
  
  METHODS
  ELISA and immunohistochemistry were applied to investigate the expression of LL-37 in induced sputum and lung tissue of COPD patients. Bronchial epithelial cell (BEP2D) and alveolar epithelial cell (A549) were treated with LL-37 synthesis polypeptide in vitro to assess the role of LL-37 in inflammation and apoptosis.
  
  
  RESULTS
  We found that increased induced sputum levels of LL-37 in COPD patients were associated with airflow limitation, health status and exercise tolerance and the expressing intensity of LL-37 in both airway district and pulmonary alveoli area in COPD group significantly increased compared with control group. Through stimulation by CSE and LPS, the expression of LL-37 was increased in bronchial epithelial cell and alveolar epithelial cell. LL-37 synthesis polypeptide can promote the releasing of inflammatory factor IL-8 and induce apoptosis of bronchial epithelial cell and alveolar epithelial cell.
  
  
  CONCLUSIONS
  This study suggested that LL-37 may play important role in the pathogenesis of COPD and may be a possible novel therapeutic target in COPD.
authors.affiliation: Department of Respiratory Medicine, Qilu Hospital, Shandong University, Wenhua West Road, Jinan 250012, China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Jiang
authors.forename: Wei
authors.initials: W
authors.lastname: Xiao
authors.forename: Mao-Xiang
authors.initials: MX
authors.lastname: Zhu
authors.forename: Zhi-Hua
authors.initials: ZH
authors.lastname: Yang
authors.forename: Xiu-Jie
authors.initials: XJ
authors.lastname: Pan
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.forename: Cong-Cong
authors.initials: CC
authors.lastname: Sun
authors.forename: Ying
authors.initials: Y
authors.lastname: Xing
mesh_terms: D023181:Antimicrobial Cationic Peptides / Q000378:metabolism / Q000502:physiology*; D017209:Apoptosis / Q000502:physiology; D001980:Bronchi / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007150:Immunohistochemistry; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D020545:Respiratory Mucosa / Q000378:metabolism; D012906:Smoke; D013183:Sputum / Q000737:chemistry; D062789:Tobacco Products; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014797:Vital Capacity / Q000502:physiology; D054804:Cathelicidins
chemical_list: D023181:Antimicrobial Cationic Peptides; D016209:Interleukin-8; D008070:Lipopolysaccharides; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D054804:Cathelicidins