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Role of interleukin‐1 and prostaglandin in in vitro bone resorption induced by Actinobacillus actinomycetemcomitans lipopolysaccharide
Author(s) -
Ishihara Yuichi,
Nishihara Tatsuji,
Maki Eijiro,
Noguchi Toshihide,
Koga Toshihiko
Publication year - 1991
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1991.tb01639.x
Subject(s) - calvaria , bone resorption , endocrinology , medicine , lipopolysaccharide , prostaglandin e2 , chemistry , resorption , dexamethasone , prostaglandin e , in vitro , biology , biochemistry
Lipopolysaccharide (Y4 LPS) isolated from Actinobacillus actinomycetemcomitans strain Y4 induced bone resorption in BALB/c mouse calvaria organ culture. The calcium release from LPS‐low responsive C3H/HeJ mouse calvaria by Y4 LPS was very low. Indomethacin almost completely inhibited prostaglandin E 2 (PGE 2 ) production by Y4 LPS‐stimulated BALB/c mouse calvaria, but did not suppress interleukin‐1 (IL‐1) release from the calvaria, and partially suppressed the bone resorption. Dexamethasone strongly inhibited the PGE 2 and IL‐1 production by Y4 LPS‐stimulated BALB/c mouse calvaria. as well as Y4 LPS‐induced bone resorption. Dexamethasone inhibited expression of membrane IL‐1 on osteoblastic cells stimulated with Y4 LPS, but indomethacin did not. Furthermore, anti‐IL‐1 serum partially suppressed the calcium release from Y4 LPS‐stimulated BALB/c mouse calvaria. These results suggest that both PGE 2 and IL‐1 participate in Y4 LPS‐induced bone resorption in vitro .