标题：Anti-CD11c antibody, Efalizumab attenuate ventilator-induced lung injury
作者：Pan, W. -Z.; Shi, C. -X.; Tian, M.; Yu, J. -G.
作者机构：[Pan, W. -Z.; Shi, C. -X.; Tian, M.] Qingdao Univ, Yantai Yuhuangding Hosp, Coll Med, Dept Anesthesiol, Yantai, Peoples R China.; [Yu, J. -G.] Shand 更多
通讯作者地址：[Yu, JG]Shandong Univ, Qilu Hosp, Coll Med, Dept Anesthesiol, Jinan 250100, Peoples R China.
来源：EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
关键词：Efalizumab; Ventilator-induced lung injury; Intrapulmonary inflammatory
摘要：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.; MATERIALS AND 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.