Enhanced monocyte migration and pro-inflammatory cytokine production by Porphyromonas gingivalis infection.
OBJECTIVE
Porphyromonas gingivalis, a major periodontal pathogen, has been reported to be involved in atherogenesis. In order to further understand this pathogen's link with systemic inflammation and vascular disease, we investigated its influence on murine monocytes and macrophages from three different sources.


METHODS
Concanavalin A-elicited peritoneal macrophages, peripheral blood monocyte-derived macrophages and WEHI 274.1 monocytes were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3.


RESULTS
Infection with P. gingivalis 381 markedly induced monocyte migration and significantly enhanced production of the pro-inflammatory cytokines, tumor necrosis factor-alpha and interleukin-6. Consistent with a role for this pathogen's major fimbriae and/or its invasive capacity, infection with DPG3 had a minimal effect on both monocyte attraction and pro-inflammatory cytokine production.


CONCLUSIONS
Since monocyte recruitment and activation are important steps in the development of vascular inflammation and atherosclerosis, these results suggest that P. gingivalis infection may be involved in these processes.
Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY 10032, USA.
A
A
Pollreisz
Y
Y
Huang
G A
GA
Roth
B
B
Cheng
M
M
Kebschull
P N
PN
Papapanou
A M
AM
Schmidt
E
E
Lalla
D000818:Animals; D001431:Bacteriological Techniques; D016866:Bacteroidaceae Infections / Q000276:immunology*; D018929:Cell Culture Techniques; D002460:Cell Line; D002465:Cell Movement / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000276:immunology*; D003208:Concanavalin A / Q000494:pharmacology; D016207:Cytokines / Q000276:immunology*; D010861:Fimbriae, Bacterial / Q000235:genetics; D006937:Hypercholesterolemia / Q000097:blood; D018836:Inflammation Mediators / Q000276:immunology*; D015850:Interleukin-6 / Q000032:analysis / Q000276:immunology; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008934:Mitogens / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D009154:Mutation / Q000235:genetics; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000276:immunology
D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D008934:Mitogens; D014409:Tumor Necrosis Factor-alpha; D003208:Concanavalin A