Increased release of IL-12p70 by monocytes after periodontal therapy.
OBJECTIVE
It has been suggested that periodontal inflammation may result in an altered immune response. The peripheral immune capacity in periodontitis patients can be investigated using lipopolysaccharide (LPS)-stimulated whole blood cell cultures (WBCC), known to reflect the behavior of monocytes in particular. A previous study in our laboratory revealed that monocytes in the stimulated cultures from periodontitis patients behaved functionally different compared with controls. The present study investigated whether this different response of periodontitis patients' monocytes is intrinsic or acquired.


METHODS
The release of inflammatory mediators was measured in Escherichia coli LPS-stimulated WBCC from 12 periodontitis patients before and after periodontal therapy. In addition, the total leukocyte and leukocyte differentiation counts were also determined in the patients before and after therapy.


RESULTS
The levels of interleukin (IL)-12p70 in cell culture supernatants increased two times and those of prostaglandin E2 showed a trend towards reduction after therapy, whereas the levels of IL-1beta, IL-6, IL-8, IL-10, IL-12p40 and tumor necrosis factor-alpha did not change. The total number of white blood cells was decreased after periodontal therapy.


CONCLUSIONS
After periodontal therapy, the functional phenotype of the peripheral blood monocytes from patients was reconstituted, resembling that of subjects without periodontitis.
Department of Periodontology, Academic Center for Dentistry Amsterdam, 1066 EA Amsterdam, the Netherlands.
S J
SJ
Fokkema
B G
BG
Loos
C
C
de Slegte
W
W
Burger
M
M
Piscaer
Y
Y
IJzerman
U
U
Van der Velden
D000328:Adult; D015232:Dinoprostone / Q000032:analysis; D004926:Escherichia coli; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D007375:Interleukin-1 / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D018664:Interleukin-12 / Q000032:analysis* / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D010518:Periodontitis / Q000276:immunology / Q000628:therapy*; D010641:Phenotype; D021122:Protein Subunits / Q000032:analysis* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D021122:Protein Subunits; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D015232:Dinoprostone