ABILITY OF BACTERIA ASSOCIATED WITH CHRONIC INFLAMMATORY DISEASE, TO STIMULATE E-SELECTIN EXPRESSION AND PROMOTE NEUTROPHIL ADHESION

Citation
Rp. Darveau et al., ABILITY OF BACTERIA ASSOCIATED WITH CHRONIC INFLAMMATORY DISEASE, TO STIMULATE E-SELECTIN EXPRESSION AND PROMOTE NEUTROPHIL ADHESION, Infection and immunity, 63(4), 1995, pp. 1311-1317
Citations number
41
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
63
Issue
4
Year of publication
1995
Pages
1311 - 1317
Database
ISI
SICI code
0019-9567(1995)63:4<1311:AOBAWC>2.0.ZU;2-O
Abstract
Porphyromonas gingivalis, Pseudomonas aeruginosa, and Helicobacter pyl ori have been shown to be associated with adult periodontal disease, c hronic lung infections, and peptic ulcers, respectively. The ability o f these bacteria to stimulate E-selectin expression and promote neutro phil adhesion, two components necessary for the recruitment of leukocy tes in response to infection, was investigated. Little or no stimulati on of E-selectin expression was observed with either P. gingivalis or H. pylori when whole cells, lipopolysaccharide (LPS), or cell wall pre parations added to human umbilical cord vein endothelial cells were ex amined. P. aeruginosa was able to induce E-selectin to near-maximal le vels; 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 bact eria did not promote endothelial cell adhesiveness by E-selectin-indep endent mechanisms. In addition, P. gingivalis LPS blocked E-selectin e xpression 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 reacti ve LPS. We suggest that this property of LPS may contribute to host ti ssue colonization, In addition, the ability of P., gingivalis to inhib it E-selectin expression may represent a new virulence factor for this organism.