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Báo cáo y học: " Overexpression of sICAM-1 in the Alveolar Epithelial "

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Overexpression of sICAM-1 in the Alveolar Epithelial ". | Mendez et al. Respiratory Research 2011 12 12 http respiratory-research.eom content 12 1 12 RESPIRATORY RESEARCH RESEARCH Open Access Overexpression of sICAM-1 in the Alveolar Epithelial Space Results in an Exaggerated Inflammatory Response and Early Death in Gram Negative Pneumonia 1 2 2 2 2 2 4 Michael P Mendez Yeni K Monroy Ming Du Angela M Preston Leslie Tolle Yujing Lin Kelli L VanDussen Linda C Samuelson4 Theodore J Standiford3 Jeffery L Curtis2 3 James M Beck2 3 Paul J Christensen2 3 Robert Paine III5 6 Abstract Background A sizeable body of data demonstrates that membrane ICAM-1 mICAM-1 plays a significant role in host defense in a site-specific fashion. On the pulmonary vascular endothelium mICAM-1 is necessary for normal leukocyte recruitment during acute inflammation. On alveolar epithelial cells AECs we have shown previously that the presence of normal mICAM-1 is essential for optimal alveolar macrophage AM function. We have also shown that ICAM-1 is present in the alveolar space as a soluble protein that is likely produced through cleavage of mICAM-1. Soluble intercellular adhesion molecule-1 sICAM-1 is abundantly present in the alveolar lining fluid of the normal lung and could be generated by proteolytic cleavage of mICAM-1 which is highly expressed on type I AECs. Although a growing body of data suggesting that intravascular sICAM-1 has functional effects little is known about sICAM-1 in the alveolus. We hypothesized that sICAM-1 in the alveolar space modulates the innate immune response and alters the response to pulmonary infection. Methods Using the surfactant protein C SPC promoter we developed a transgenic mouse SPC-sICAM-1 that constitutively overexpresses sICAM-1 in the distal lung and compared the responses of wild-type and SPC-sICAM-1 mice following intranasal inoculation with K. pneumoniae. Results SPC-sICAM-1 mice demonstrated increased mortality and increased systemic dissemination of organisms compared with wild-type mice. We also found