title: Enhancement of lipopolysaccharide-stimulated PGE2 and IL-1beta production in gingival fibroblast cells from old rats.
abstract: The effect of aging on gingival fibroblasts in response to bacterial infection was studied. Rat gingival fibroblast (rGF) cells were cultured from gingival tissue removed from young (6 weeks old) and old (20 months old) rats. Both types of rGF cells were challenged with lipopolysaccharide (LPS) from the periodontal pathogen Campylobacter rectus. The levels of prostaglandin E2 (PGE2) and interleukin 1beta (IL-1beta) released into the cultured medium were measured by a specific radioimmunoassay. LPS stimulated PGE2 and IL-1beta production in a dose-and time-dependent manner in rGF cells from both young and old rats was seen. Production of PGE2 and IL-1beta by rGF cells from the old rats was higher than those from the young in response to LPS. This greater ability from the older rGF cells to produce PGE2 and IL-1beta was due to higher mRNA levels of cyclooxygenase 2 and IL-1beta, respectively. In contrast, cyclooxygenase-1 and IL-1beta converting enzyme gene mRNA levels remained unchanged. Because LPS-stimulated PGE2 and IL-1beta production was enhanced by in vivo cellular aging, aging of GF may affect the severity of inflammation and bone resorption by producing a large amount of PGE2 and IL-1beta in response to bacterial infection.
authors.affiliation: Department of Biochemistry, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Okamura
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Abiko
mesh_terms: D000368:Aged; D000375:Aging / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D001483:Base Sequence; D002167:Campylobacter / Q000472:pathogenicity; D002169:Campylobacter Infections / Q000276:immunology / Q000378:metabolism; D051546:Cyclooxygenase 2; D017931:DNA Primers / Q000235:genetics; D015232:Dinoprostone / Q000096:biosynthesis*; D005347:Fibroblasts / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D005881:Gingiva / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D008565:Membrane Proteins; D010518:Periodontitis / Q000209:etiology; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016388:Tooth Loss / Q000209:etiology
chemical_list: D017931:DNA Primers; D007375:Interleukin-1; D007527:Isoenzymes; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D012333:RNA, Messenger; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone