Ability of bacteria associated with chronic inflammatory disease to stimulate E-selectin expression and promote neutrophil adhesion

Abstract

Porphyromonas gingivalis, Pseudomonas aeruginosa, and Helicobacter pylori have been shown to be associated with adult periodontal disease, chronic lung infections, and peptic ulcers, respectively. The ability of these bacteria to stimulate E-selectin expression and promote neutrophil adhesion, two components necessary for the recruitment of leukocytes in response to infection, was investigated. Little or no stimulation of E-selectin expression was observed with either P. gingivalis or H. pylori when whole cells, lipopolysaccharide (LPS), or cell wall preparations added to human umbilical cord vein endothelial cells were examined. P. aeruginosa was able to induce E-selectin to near-maximal levels; however, it required approximately 100 to 1,000 times more whole cells or LPS than that required by E. coli. Neutrophil-binding assays revealed that LPS and cell wall preparations obtained from these bacteria did not promote endothelial cell adhesiveness by E-selectinindependent mechanisms. In addition, P. gingivalis LPS blocked E-selectin expression by LPS obtained from other bacteria. We propose that lack of E-selectin stimulation and the inability to promote endothelial cell adhesiveness are two additional indications of low biologically reactive LPS. We suggest that this property of LPS may contribute to host tissue colonization. In addition, the ability of P. gingivalis to inhibit E-selectin expression may represent a new virulence factor for this organism.

Porphyromonas gingivalis lipopolysaccharide lipid A heterogeneity: differential activities of tetra- and penta-acylated lipid A structures on E-selectin expression and TLR4 recognition

“…3). Consistent with our previous observations over a wide dose range of LPS (Darveau et al ., 1995;Coats et al ., 2003), PgLPS 1435/1449 did not elicit a strong E-selectin protein (Fig. 3A) or RNA ( Fig.…”

“…HUVEC stimulation media is Medium 199 supplemented with 4 mM glutamine, 90 µg ml −1 heparin, 1 mM sodium pyruvate, 1 mg ml −1 human serum albumin and 5-10% human serum (Gemini Bioproducts, Calabasas, CA). In some experiments CD14-depleted serum was employed and it was prepared as described previously (Darveau et al, 1995).…”

Fimbria-dependent activation of pro-inflammatory molecules in Porphyromonas gingivalis infected human aortic endothelial cells

“…In contrast, E. coli LPS was able to induce significant expression of ICAM-1, but only weak expression of VCAM-1 and P-selectin. These findings are in partial disagreement with previous studies whose results demonstrated E. coli LPS stimulation of all three CAMs (Kapiotis et al, 1994;Darveau et al, 1995). It should be noted that these studies utilized HUVEC and, as mentioned previously, several groups have shown differences in the responsiveness and gene expression patterns between arterial and venous endothelial cells.…”

The anti‐endotoxic effects of the KSL‐W decapeptide on Escherichia coli O55:B5 and various oral lipopolysaccharides

“…E-selectin expression was evaluated in human umbilical vein endothelial cells after 4 h of exposure to either E. coli lipopolysaccharide alone or to E. coli lipopolysaccharide pre-incubated with KSL-W. Similarly to previous reports using lipopolysaccharide (28,40,41), we observed consistent E-selectin responses within the human umbilical vein endothelial cells assay system that required as little as 1-100 ng/mL of E. coli lipopolysaccharide to yield a significant response. Optimization assays revealed that this concentration (10 ng; E. coli O55:B5) was in the middle of the linear stimulation range for E-selectin expression in human umbilical vein endothelial cells and was therefore used as the stimulation dose.…”