Pathogen-accelerated atherosclerosis occurs early after exposure and can be prevented via immunization.
Here we report on early inflammatory events associated with Porphyromonas gingivalis-accelerated atherosclerosis in apolipoprotein E knockout (ApoE-/-) mice. Animals challenged with P. gingivalis presented with increased macrophage infiltration, innate immune marker expression, and atheroma without elevated systemic inflammatory mediators. This early local inflammatory response was prevented in mice immunized with P. gingivalis. We conclude that localized up-regulation of innate immune markers early after infection, rather than systemic inflammation, contributes to pathogen-accelerated atherosclerosis.
Miyamoto
Takanari
T
Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Evans Biomedical Research Center, Room 637, 650 Albany St., Boston, MA 02118, USA.
Yumoto
Hiromichi
H
Takahashi
Yusuke
Y
Davey
Michael
M
Gibson
Frank C
FC
Genco
Caroline Attardo
CA
D000818:Animals; D001013:Aorta, Thoracic / Q000276:immunology / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D050197:Atherosclerosis / Q000382:microbiology* / Q000473:pathology / Q000517:prevention & control*; D016866:Bacteroidaceae Infections / Q000150:complications* / Q000276:immunology / Q000382:microbiology; D007113:Immunity, Innate; D007114:Immunization; D007249:Inflammation / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control; D008297:Male; D051379:Mice; D016966:Porphyromonas gingivalis / Q000276:immunology* / Q000472:pathogenicity; D013997:Time Factors
D001057:Apolipoproteins E