Journal
INFECTION AND IMMUNITY
Volume 69, Issue 3, Pages 1477-1482Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.69.3.1477-1482.2001
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Funding
- NCI NIH HHS [5P30-CA-42014, P30 CA042014] Funding Source: Medline
- NIAID NIH HHS [R37 AI018797, AI-18797, AI-3223, R56 AI018797, R01 AI032223, R01 AI018797, R56 AI032223] Funding Source: Medline
- NIDCR NIH HHS [DE-08228] Funding Source: Medline
- NIGMS NIH HHS [R01 GM050870, GM-50870] Funding Source: Medline
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Lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants, More importantly, TLR2 stimulation by this P. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages by Escherichia coli LPS. These data suggest that (i) P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively, Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.
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