Cigarette smoking is associated with increased incidence of periodontal disease and poor response to therapy. In the present study, we examined the effects of nicotine on several functions of periodontal ligament fibroblasts (PDLF): proliferation, attachment, alkaline phosphatase production and chemotaxis. Nicotine concentrations varying from 5 ng/ml to 250 microg/ml were tested. Proliferation of cells was studied by the incorporation of 3H-thymidine, and a dose-dependent inhibition was observed with concentrations > or =100 ng/ml. Similar results were observed when studying the attachment of the cells on plastic surfaces, using a colorimetric method. The inhibition of attachment was even more evident after 6 h incubation of the cells with nicotine. The activity of alkaline phosphatase, as determined with the substrate p-nitrophenyl phosphate, in both conditioned medium (CM) and cellular extract (CE), was also significantly decreased in a concentration-related fashion. Finally, the chemotaxis of PDLE as examined by a modification of the Boyden's blind-well chamber technique, was inhibited in a dose-dependent manner. The degree of inhibition varied from 15% with the lowest concentration of nicotine (50 ng/ml), to almost 90% with the highest (5 microg/ml). The results show that nicotine can have direct adverse effects on various functions of the periodontal cells.

SUMMARY lnterfcron (IFN) alpha :ind gamma were measured by radio-immunoassays in supernatants from cultures of peripheral blood mononuclear cells (PBMC) or purified T cell subsets incubated wilh either Plasmodium faUiparum schizont-enriched malaria antigen (mAg), uninfected red blood ceils (RBC) or pokewced mitogen (PWM). Cell donors were 24 clinically immune, healthy AfHean adult native residents of a P. falciparum-endemlc region. Haut-Ogoouc. Gabon, and seven non-immune. European temporary residents with a history of a single to a few malaria inleclions during the previous I to 9 months. When PBMC were cultured in medium alone or with RBC antigen no or low titres oriFN-y were detected. PBMC proliferation and IFN-y produetion observed in the presenee of mAg were dose dependent and significantly correlated. When cultured with niAg, PBMC from nonimmune Europeans produced significantly higher levels of IFN-y than did PBMC from clinically immune Africans. No such difference was found when PBMC were cultured with PWM. The mAginduced IFN-'/ production was due mainly to CD4' T eells and was not enhanced by CDS' T cell depletion. No IFTJ-a was deteeted in culture supernatants. Thus, P. falciparum antigens are able to induce in vitro produetion of IFT^I-v by CD4'^ Tcells; however, in this sample, individuals considered to be clinically resi.stant to malaria were low producers of IFN-"/.

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