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Infection and Immunity, October 2004, p. 5910-5918, Vol. 72, No. 10
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.10.5910-5918.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Infectious Diseases,1 Department of Periodontology, Charité, CVK,2 Robert Koch-Institut, Berlin, Germany,3 Department of Oral Biology, Boston University Goldman School of Dental Medicine, Boston, Massachusetts,4 Department of Oral Biology, State University of New York, Buffalo, New York5
Received 19 February 2004/ Returned for modification 5 May 2004/ Accepted 14 July 2004
Porphyromonas gingivalis is an important bacterium involved in periodontal diseases. Colonization by periodontopathogens has been associated with severe local inflammatory reactions in the connective tissue. In this study we characterized P. gingivalis-mediated infection and activation of human umbilical vein endothelial cells by using two strains of different virulence capacities, strains ATCC 53977 and DSMZ 20709. Both strains were able to adhere to and infect endothelial cells with an infection rate of 0.48% for ATCC 53977 and 0.007% for DSMZ 20709. The triggering of two signal transduction pathways in P. gingivalis-infected endothelial cells was demonstrated for both strains, with a rapid increase of p38 mitogen-activated protein kinase phosphorylation and a more delayed degradation of I
B
, followed by nuclear translocation of NF-
B. In addition, both strains induced enhanced expression of endothelial adhesion molecules E-selectin and intracellular adhesion molecule 1 (ICAM-1). Target cell activation was independent of bacterial fimbriae expression since the fimA knockout strain A7436
fimA induced the same level of ICAM-1 as the corresponding wild type (A7436-WT). Thus, two P. gingivalis strains, ATCC 53799 and DSMZ 20709, infect endothelial cells and trigger signaling cascades leading to endothelial activation, which in turn may result in or promote severe local and systemic inflammation.
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