title: Anti-CD11c antibody, Efalizumab attenuate ventilator-induced lung injury.
abstract: BACKGROUND
  The pathophysiology of ventilator-induced lung injury (VILI) involves multiple mechanisms including inflammation and inflammatory cells infiltration. The anti-CD11c monoclonal antibody, Efalizumab has been demonstrated to inhibit the T cell activation, migration and adhesion to keratinocytes.
  
  
  METHODS
  In this study, we induced lung injury with mechanical ventilation in male Sprague-Dawley rats, the rats were divided into four groups: lung-protective ventilation (LV), injurious ventilation (HV), HV+human IgG control and HV+ Efalizumab groups. Then we detected the lung tissue wet/dry ratio, and the activity of myeloperoxidase (MPO) was determined. The concentration of protein, TNF-a, IL-6, IL-1b and MIP-2 in the BALF were detected by ELISA. The expression ICAM-1 was measured by Realtime PCR.
  
  
  RESULTS
  Compared with the human IgG control treated group, the treatment of Efalizumab attenuate the ventilator-induced lung injury, including the wet/dry ratio and the activity of myeloperoxidase (MPO), meanwhile, the level of pro-inflammatory cytokines, such as TNF-a, IL-6, IL-1b and MIP-2 were decreased in the BALF of Efalizumab-treated group rats compared with the human IgG-treated control group. In addition, the histopathological index of ventilator-induced lung injury was improved after efalizumab treatment, that also reduced the recruitment of inflammatory cells into the lung, such as neutrophils.
  
  
  CONCLUSIONS
  Our data suggested that Efalizumab could protect rat from ventilator-induced lung injury and improve the survival time through the inhibition of intrapulmonary inflammatory response.
authors: Department of Anesthesiology, Yantai Yuhuangding Hospital, Medical College, Qingdao University, Yantai, China. yujingyjg@163.com.
authors: W-Z
authors: WZ
authors: Pan
authors: C-X
authors: CX
authors: Shi
authors: M
authors: M
authors: Tian
authors: J-G
authors: JG
authors: Yu
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D039521:CD11c Antigen / Q000378:metabolism*; D054426:Chemokine CXCL2 / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009195:Peroxidase / Q000378:metabolism; D011654:Pulmonary Edema / Q000188:drug therapy / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055397:Ventilator-Induced Lung Injury / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D039521:CD11c Antigen; D054426:Chemokine CXCL2; C513296:Cxcl2 protein, rat; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; C472181:efalizumab