[Effects of the serum obtained from smoke inhalation injury rats on PMN adhesion and transmigration in vitro].

Objective: This study was conducted to determine the changes in PMN adhesive capacity to endothelial cells and transmigration through endothelial cell (CEC) sheet in the presence of the serum from rats with smoke inhalation injury (SII). The effects of adhesion molecules CD11a, CD11b, and ICAM-1 on the PMN adhesion and transmigration were also studied.

Method: In the present study fluorescent assay, EC sheet cultured on the 5 microns permeable membrane and antibody blocking technique were used to study the PMN adhesion and transmigration in vitro.

Result: It was found that the serum from SII rats could promote PMN adhesion to CEC sheet. After being cultured with the serum for 12-24 h, PMN adhesion to CEC was more than three times of that in control. The serum also enhanced PMN transmigration through the CEC sheet in vitro, doubling the amount observed in control when the sheet was cultured with the serum for 24 h. Based on the above data it was believed that the SII rat serum could enhance PMN adhesion to and transmigration through lung capillary, and the percentages of PMN adhesion and transmigration were found to be positively correlated (r = 0.975). Furthermore, the antibodies against CD11a, CD11b, and ICAM-1 reduced PMN adhesion 44%, 55% and 51%, respectively, and at the same time decreased PMN transmigration 39%, 65%, and 58%, respectively.

Conclusion: In the presence of serum obtained from SII rats PMN adhesion to and transmigration through CEC sheet increased, which is the possible underlying mechanism responsible for PMN infiltration in vitro. Moreover, the adhesion molecules such as CDA11a, CD11b, and ICAM-1 play an important role in the process. Infiltrated PMN could release oxygen free radicals and protease to injure lung tissue.