Effect Of Recombinant β-defensin 2 On Changers Of Pulmonary ICAM-1 On Acute Lung Injury

BacgroundThe acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that may occur in any patient without any predisposition and that is mostly triggered by underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia with a PaO2/FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%) and relatively frequent (incidence between 13.5 per 100,000 to 75 per 100,000). Acute lung injury (ALI) describes a similar, but less severe, clinical condition, with PaO2/FiO2 values between 200 and 300 mmHg. Despite ongoing and intensive scientific research in this area, the mechanisms underlying ALI/ARDS are still not completely understood, and until recently, there were no studies demonstrating any beneficial effect of a single treatment modality in ARDS.Intercellular adhesion molecule (ICAM)-l (CD54) is a member of the immunoglobulin gene superfamily and is expressed on endothelial cells, epithelial cells, and fibroblasts, as well as T-cells, B-cells, dendritic cells, macrophages, and eosinophils. Intercellular adhesion molecule (ICAM)-l has recently attracted much interest in view of increasing evidence that it plays a prominent role in lung diseases.ï¿¡ -defensin 2 is a small molecule anti-microbial peptide located in a lot of tissue include skin and lungs. Recent studies showed that the small peptide is of particular importance to innate immune response and acquired immune response against microbial infection. It is helpful to further explore pathogenesis and pharmaceutical for ALI/ ARDS that clarifying the effect and mechanism of 0 -defensin 2 on the lungs. ObjectiveTo investigate the effect of recombinant 3 -defensin 2 peptide on expression of Pulmonary IC AM-1 in rat with Acute Lung Injury (ALI). Materials and MethodsSixty SD male rats weighting 250-300g were randomly divided into two groups, controls and defensin group. 5 X 105PFU adenovirus with or without the ï¿¡ -defensin 2 gene wastitrated into trachea via intubation, respectively, 48h before CLP. Lungs were harvested at Oh, 12h, 24h, 36h and 72h following CLP. Immunohistochemistry was performed to detect the expression of ICAM-1, data was analyzed quantitatively with Image Pro-Plus5.0, level of ICAM-1 was presented as average density of light. ResultsCompared with the basic expression of ICAM-1 in lung tissues in healthy rat, the level of ICAM-1 in lung tissue in ALI rat increased significantly at 24h and 36h after CLP in controls, while it didn't show difference at observed time-point in defensin group. Furthermore, compared with that in controls, the level of ICAM-1 in lung tissue in defensin group showed a marked decrease at 24h and 36h after CLP. ConclusionThe increased expression of ICAM-1 in lung tissue in ALI rat can be modulated by recombinant 3 -defensin 2 peptide, it may suggest that P -defensin 2 play a protective role on the injuried lung in ALI.