Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study.
BACKGROUND
Inflammation is a significant component of atherosclerosis lesions. Bacteria, including periodontopathogens, have been demonstrated in atherosclerotic plaques and cross-reactivity of the immune response to bacterial GroEL with human heat shock protein 60 has been suggested as a link between infections and atherosclerosis.


METHODS
In this study, the nature of the inflammatory infiltrate and the presence of human heat shock protein 60 and GroEL were examined in 31 carotid endarterectomy specimens. Additionally, monoclonal antibodies were used to detect the presence of six bacteria, including those implicated in periodontal disease.


RESULTS
The inflammatory cell infiltrate of the lesions was dominated by CD14(+) macrophages and CD4(+) T cells. Most cells of the infiltrate as well as the endothelium were HLA-DR(+), indicating activation; however, there was an absence of CD25 expression, demonstrating that the activated T cells were not proliferating. Few CD1a(+) and CD83(+) cells were noted. Human heat shock protein 60 expression was evident on endothelial cells and cells with the appearance of smooth muscle cells and lymphocytes. GroEL and bacteria were detected within intimal cells. Chlamydia pneumoniae, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia, Prevotella intermedia, and Actinobacillus actinomycetemcomitans were found in 21%, 52%, 34%, 34%, 41%, and 17% of arteries, respectively.


CONCLUSIONS
These results give evidence for a specific immune response associated with atherosclerosis. Whether bacteria initiate the observed inflammation in atherosclerotic lesions is not clear; however, the present study shows that maintenance of inflammation may be enhanced by the presence of periodontopathic bacteria.
Ford
P J
PJ
Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia. p.ford@uq.edu.au
Gemmell
E
E
Chan
A
A
Carter
C L
CL
Walker
P J
PJ
Bird
P S
PS
West
M J
MJ
Cullinan
M P
MP
Seymour
G J
GJ
D016976:Aggregatibacter actinomycetemcomitans / Q000302:isolation & purification; D015703:Antigens, CD / Q000032:analysis; D018949:Antigens, CD1 / Q000032:analysis; D050197:Atherosclerosis / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D001439:Bacteroides / Q000302:isolation & purification; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology; D018834:Chaperonin 60 / Q000032:analysis*; D016993:Chlamydophila pneumoniae / Q000302:isolation & purification; D016894:Endarterectomy, Carotid; D042783:Endothelial Cells / Q000473:pathology; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology; D016967:Fusobacterium nucleatum / Q000302:isolation & purification; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000473:pathology; D008562:Membrane Glycoproteins / Q000032:analysis; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D010510:Periodontal Diseases / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000302:isolation & purification; D018713:Prevotella intermedia / Q000302:isolation & purification; D017539:Tunica Intima / Q000382:microbiology; D000097802:CD83 Antigen
D015703:Antigens, CD; D018949:Antigens, CD1; D018834:Chaperonin 60; D006684:HLA-DR Antigens; D007136:Immunoglobulins; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D000097802:CD83 Antigen; C419393:CD1a antigen