PAF levels in saliva are regulated by inflammatory cells.
Platelet activating factor (PAF), a powerful inflammatory phospholipid mediator, has been detected in normal human saliva and found to be increased in periodontitis. The cellular source of PAF in saliva is controversial although several data suggest an origin related to the presence of inflammatory cells. PAF levels in biological fluids are regulated by PAF-producing cells and by the PAF-degrading acetylhydrolase. Although in normal human saliva acetylhydrolase activity is very low, no information is available on the levels of this enzyme in inflammatory conditions of the mouth. The aim of our study was to assess the contribution of inflammatory cells to the levels of PAF in saliva in normal subjects and in patients with periodontitis. PAF was measured by radioimmunoassay (RIA) in mixed uncentrifuged saliva and in cell-free saliva from healthy subjects, before and after tooth brushing, and in patients with periodontitis. In healthy subjects PAF levels were significantly higher in whole saliva than in centifuged saliva (1.51 +/- 0.22 vs. 0.92 +/- 0.04 ng/ml, p < 0.0039). A significant increase in the amount of PAF was detected in whole saliva, but not in centifuged saliva, 2 h after tooth brushing. In patients with periodontitis PAF levels were not different from those of healthy individuals when using centrifuged saliva but were significantly higher when using whole, uncentrifuged saliva. Exogenous radiolabelled PAF was degraded much more rapidly by the saliva of periodontitis patients than by that of normal subjects. In conclusion, our study shows that inflammatory cells regulate the levels of PAF in saliva contributing to its production and degradation. The differential degradation of PAF in normal and inflammatory saliva highlights the absolute need of a series of methodological precautions when performing studies on salivary PAF.
Ribaldi
E
E
Institute of Internal and Vascular Medicine, University of Perugia, Italy.
Guerra
M
M
Mezzasoma
A M
AM
Staffolani
N
N
Goracci
G
G
Gresele
P
P
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000328:Adult; D000704:Analysis of Variance; D002474:Cell-Free System; D002498:Centrifugation; D005260:Female; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000201:enzymology / Q000378:metabolism; D010741:Phospholipases A / Q000032:analysis; D010972:Platelet Activating Factor / Q000032:analysis* / Q000378:metabolism; D011863:Radioimmunoassay; D012463:Saliva / Q000737:chemistry* / Q000201:enzymology; D014099:Toothbrushing
D018836:Inflammation Mediators; D010972:Platelet Activating Factor; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase