2001 Volume 43 Issue 3 Pages 260-272
The periodontal disease is believed to worsen due to inflammation and destruction of periodontal tissue caused by bacterial endotoxin lipopolysaccharide (LPS) released by the breakdown of bacteria due to a biological reaction between Gram negative bacteria and polymorphonuclear leukocytes (PMN) that migrate to the infection site. To study the effects of LPS on PMN, we pretreated PMN with E. coli-derived LPS and examined PMN phagocytic ability, Fcγ receptors, and C 3 bi receptors using flow cytometry (FCM) and confocal laser scanning microscopy (CLSM), with the following results :
1) The phagocytic rate increased significantly in the 0.01mg/ml and 0.1mg/ml LPS groups compared to the control group, while a significant decrease occurred in the 10 mg/ml LPS group.
2) The degree of phagocytosis significantly increased in the 0.01mg/ml and 0.1 mg/ml LPS groups compared to the control group.
3) The expression of Fcγ receptors tended to increase LPS-dose-dependently, with a significant decrease in the 10 mg/ml LPS group compared to the control group.
4) The expression of Fc. A receptors tended to increase LPS-dose-dependently, with a significant decrease in the 10mg/ml LPS group compared to the control group.
5) Continuous tomography of bead-ingesting phagocytes using CLSM showed beads inside cells and on the cell surface.
6) CLSM revealed Fcγreceptors are present uniformly throughout the entire cell membrane, while C 3 bi receptors were observed at several locations on the cell membrane.
Oun results thus show important differences in where foreign substances adhere to the PMN surface and when they are taken up into PMNs during PMN phagocytosis. They also shed light on location, in PMN receptors. J. Jpn. Soc. Periodontol., 43: 260-272, 2001.
