Bacteroides gingivalis stimulates bone resorption via interleukin‐1 production by mononuclear cells The relative role for B. gingivalis endotoxin

AAB Noorloos, JWM van der Meer… - Journal of clinical …, 1990 - Wiley Online Library
AAB Noorloos, JWM van der Meer, JS van de Gevel, E Schepens, TJM van Steenbergen…
Journal of clinical periodontology, 1990Wiley Online Library
Supernatants of human peripheral blood mononuclear cells cultured in the presence of B.
gingivalis, showed a strong osteoclast stimulating activity as measured by 45Ca release
from fetal mouse long bones in vitro. These supernatants also contained a high
concentration of bioactive and immunoreactive interleukin‐l (IL‐1), but tumor necrosis factor
(TNFa), another osteoclast‐activating cytokine, was not detected. Osteoclast activation by
the supernatants was inhibited by an antibody against IL‐1. whereas ultrapure human IL‐1 …
Abstract
Supernatants of human peripheral blood mononuclear cells cultured in the presence of B. gingivalis, showed a strong osteoclast stimulating activity as measured by 45Ca release from fetal mouse long bones in vitro. These supernatants also contained a high concentration of bioactive and immunoreactive interleukin‐l (IL‐1), but tumor necrosis factor (TNFa), another osteoclast‐activating cytokine, was not detected. Osteoclast activation by the supernatants was inhibited by an antibody against IL‐1. whereas ultrapure human IL‐1 mimicked the effect of the supernatant. The ability of B. gingivalis to induce IL‐1 and OAF production was heat sensitive, as 20 min heating of the bacteria at 120°C caused a 50% loss of activity. In addition, purified B. gingivalis lipopolysaccharide (LPS) had little IL‐1 inducing capacity, compared with LPS of Escherichia coli. These data suggest that human peripheral blood cells confronted with B. gingivalis produce large amounts of IL‐1 which has strong osteoclast stimulating activity. However, in contrast with E. coli LPS, B. gingivalis LPS does not seem to be the major inducing agent. Thus other bacterial components must be responsible for the observed IL‐1 and OAF induction.
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