title: Infliximab protects against pulmonary emphysema in smoking rats.
abstract: BACKGROUND
  It is widely accepted that tumor necrosis factor-α (TNF-α) plays an important role in the pathogenesis of emphysema. This study aimed at investigating the protective effects of anti-TNF-α antibody, infliximab, in the development of emphysema induced by passive smoking in rats.
  
  
  METHODS
  Thirty-nine rats were randomly divided into a normal control group (group 1), an emphysema group (group 2), and an infliximab-intervention group (group 3). Rat models of emphysema were established by exposure to cigarette smoking daily for 74 days. After 1 month, the infliximab intervention group was treated with infliximab via subcutaneous injection. The levels of TNF-α, IL-8 and vascular endothelial growth factor (VEGF) in bronchoalveolar lavage fluid (BALF) were measured with enzyme linked immunosorbent assay (ELISA). The number and classification of cells in the BALF were measured. Lung tissue sections stained by hematoxylin and eosin (HE) were observed, and mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were used to examine the percentage of positive cells and distribution of apoptotic cells.
  
  
  RESULTS
  The levels of TNF-α and IL-8 in BALF were higher in group 2 than in group 1 and group 3. The MLI was greater in group 2 than that in group 1 and group 3 while MAN was decreased. The concentration of VEGF in BALF of group 2 was significantly decreased as compared with group 1. The total cells and neutrophils number was significantly increased in group 2 as compared with group 1 and group 3, so was the percentage of neutrophils. The number of TUNEL positive cells in the alveolar septa was significantly increased in group 2 as compared with group 1 and group 3.
  
  
  CONCLUSIONS
  Infliximab protects against cigarette smoking-induced emphysema by reducing airway inflammation, attenuating alveolar septa cell apoptosis and improving pathological changes.
authors.affiliation: Department of Respiratory Medicine, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, China.
authors.forename: Xiang-Yan
authors.initials: XY
authors.lastname: Zhang
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Qian-Yun
authors.initials: QY
authors.lastname: Sun
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.forename: Rong-Rong
authors.initials: RR
authors.lastname: Luo
authors.forename: Zi-Fen
authors.initials: ZF
authors.lastname: Wan
authors.forename: Xian-Wei
authors.initials: XW
authors.lastname: Ye
authors.forename: Wei-Jia
authors.initials: WJ
authors.lastname: Liu
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Rao
authors.forename: Jing
authors.initials: J
authors.lastname: Han
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D000069285:Infliximab; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D011650:Pulmonary Alveoli / Q000166:cytology / Q000187:drug effects; D011656:Pulmonary Emphysema / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D016209:Interleukin-8; D014028:Tobacco Smoke Pollution; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab