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Infect Immun, June 1998, p. 2736-2742, Vol. 66, No. 6
Department of Periodontology, Hebrew
University-Hadassah School of Dental Medicine, Jerusalem,
Israel,1 and
Department of Oral Biology
and Periodontology, Goldman School of Dental Medicine, Boston
University, Boston, Massachussetts2
Received 11 August 1997/Returned for modification 21 October
1997/Accepted 6 March 1998
Porphyromonas gingivalis is one of the pathogens
associated with periodontal diseases, and its lipopolysaccharide (LPS)
has been suggested as a possible virulence factor, acting by
stimulation of host cells to secrete proinflammatory mediators.
However, recent studies have shown that P. gingivalis LPS
inhibited some components of the inflammatory response. The present
study was designed to test the hypothesis that there are
strain-dependent variations in the ability of P. gingivalis
LPS to elicit the host inflammatory response. By using LPS preparations
from two strains of P. gingivalis, W50 and A7346, the
responses of mouse macrophages and human monocytes were evaluated by
measuring the secretion of nitric oxide (NO) and tumor necrosis factor
alpha (TNF-
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Strain-Dependent Activation of Monocytes and
Inflammatory Macrophages by Lipopolysaccharide of
Porphyromonas gingivalis
). Both direct and indirect (priming) effects were
investigated. LPS from Salmonella typhosa was used as a
reference LPS. P. gingivalis A7436 LPS induced lower secreted levels of NO from the tested cells than S. typhosa
LPS but induced similar levels of TNF-
. In contrast, LPS from
P. gingivalis W50 did not induce NO or TNF-
secretion.
Preincubation of macrophages with LPS from S. typhosa or
P. gingivalis A7436 prior to stimulation with S. typhosa LPS upregulated NO secretion and downregulated TNF-
secretion, while preincubation with P. gingivalis W50 LPS
enhanced both TNF-
and NO secretory responses. These results
demonstrate that LPSs derived from different strains of P. gingivalis vary in their biological activities in vitro. The
findings may have an impact on our understanding of the range of
P. gingivalis virulence in vivo.
*
Corresponding author. Mailing address: Department of
Periodontology, Hebrew University-Hadassah School of Dental Medicine, P.O. Box 12272, Jerusalem 91120, Israel. Phone: 972-2-6777826. Fax:
972-2-6438705. E-mail: shapiral{at}cc.huji.ac.il.
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