title: 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-selectin-independent 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.
authors.affiliation: Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121.
authors.forename: R P
authors.initials: RP
authors.lastname: Darveau
authors.forename: M D
authors.initials: MD
authors.lastname: Cunningham
authors.forename: T
authors.initials: T
authors.lastname: Bailey
authors.forename: C
authors.initials: C
authors.lastname: Seachord
authors.forename: K
authors.initials: K
authors.lastname: Ratcliffe
authors.forename: B
authors.initials: B
authors.lastname: Bainbridge
authors.forename: M
authors.initials: M
authors.lastname: Dietsch
authors.forename: R C
authors.initials: RC
authors.lastname: Page
authors.forename: A
authors.initials: A
authors.lastname: Aruffo
mesh_terms: D001424:Bacterial Infections / Q000276:immunology*; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D002473:Cell Wall / Q000276:immunology; D002478:Cells, Cultured; D002908:Chronic Disease; D019040:E-Selectin; D004730:Endothelium, Vascular / Q000473:pathology; D004926:Escherichia coli / Q000276:immunology; D005786:Gene Expression Regulation; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology*; D016966:Porphyromonas gingivalis / Q000276:immunology / Q000472:pathogenicity*; D011550:Pseudomonas aeruginosa / Q000276:immunology / Q000472:pathogenicity*; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D008070:Lipopolysaccharides; D012333:RNA, Messenger