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Fusobacterium nucleatum Alters Atherosclerosis Risk Factors and Enhances Inflammatory Markers with an Atheroprotective Immune Response in ApoE() Mice.

Velsko IM, Chukkapalli SS, Rivera-Kweh MF, Chen H, Zheng D, Bhattacharyya I, Gangula PR, Lucas AR, Kesavalu L - PLoS ONE (2015)

Bottom Line: The American Heart Association supports an association between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) but does not as of yet support a causal relationship.Chronic oral infection established F. nucleatum colonization in the oral cavity, induced significant humoral IgG (P=0.0001) and IgM (P=0.001) antibody response (12 and 24 weeks), and resulted in significant (P=0.0001) alveolar bone resorption and intrabony defects.Despite evidence for systemic infection in several organs and modulation of known atherosclerosis risk factors, aortic atherosclerotic lesions were significantly reduced after F. nucleatum infection suggesting a potential protective function for this member of the oral microbiota.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontology, College of Dentistry, University of Florida, Gainesville, Florida, United States of America.

ABSTRACT
The American Heart Association supports an association between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) but does not as of yet support a causal relationship. Recently, we have shown that major periodontal pathogens Porphyromonas gingivalis and Treponema denticola are causally associated with acceleration of aortic atherosclerosis in ApoE hyperlipidemic mice. The aim of this study was to determine if oral infection with another significant periodontal pathogen Fusobacterium nucleatum can accelerate aortic inflammation and atherosclerosis in the aortic artery of ApoE mice. ApoE mice (n = 23) were orally infected with F. nucleatum ATCC 49256 and euthanized at 12 and 24 weeks. Periodontal disease assessments including F. nucleatum oral colonization, gingival inflammation, immune response, intrabony defects, and alveolar bone resorption were evaluated. Systemic organs were evaluated for infection, aortic sections were examined for atherosclerosis, and inflammatory markers were measured. Chronic oral infection established F. nucleatum colonization in the oral cavity, induced significant humoral IgG (P=0.0001) and IgM (P=0.001) antibody response (12 and 24 weeks), and resulted in significant (P=0.0001) alveolar bone resorption and intrabony defects. F. nucleatum genomic DNA was detected in systemic organs (heart, aorta, liver, kidney, lung) indicating bacteremia. Aortic atherosclerotic plaque area was measured and showed a local inflammatory infiltrate revealed the presence of F4/80+ macrophages and CD3+ T cells. Vascular inflammation was detected by enhanced systemic cytokines (CD30L, IL-4, IL-12), oxidized LDL and serum amyloid A, as well as altered serum lipid profile (cholesterol, triglycerides, chylomicrons, VLDL, LDL, HDL), in infected mice and altered aortic gene expression in infected mice. Despite evidence for systemic infection in several organs and modulation of known atherosclerosis risk factors, aortic atherosclerotic lesions were significantly reduced after F. nucleatum infection suggesting a potential protective function for this member of the oral microbiota.

No MeSH data available.


Related in: MedlinePlus

Chronic oral infection with F. nucleatum induced significant levels of serum F. nucleatum-specific antibodies.Graphs represent the fold-increase in F. nucleatum-specific IgG or IgM antibody titer in infected mice over control mice at both 12 and 24 weeks of infection. (*** P<0.001).
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pone.0129795.g002: Chronic oral infection with F. nucleatum induced significant levels of serum F. nucleatum-specific antibodies.Graphs represent the fold-increase in F. nucleatum-specific IgG or IgM antibody titer in infected mice over control mice at both 12 and 24 weeks of infection. (*** P<0.001).

Mentions: Serum antibody response to periodontal pathogens is further evidence of bacterial infection. ELISA antibody analysis of serum samples from 12 week-infected mice showed significantly higher IgG levels in infected mice (approximately 70-fold) than control mice (Fig 2, P = 0.0001). Similarly, IgM antibody levels in 12 week-infected mice were significantly greater (approximately 700-fold) than control mice (P = 0.0001). In addition, IgG levels of 24 week-infected mice were significantly higher (approximately 15-fold) than controls (P = 0.0001), as were IgM levels of 24 week-infected mice (approximately 700-fold) than controls (P = 0.001) (Fig 2).


Fusobacterium nucleatum Alters Atherosclerosis Risk Factors and Enhances Inflammatory Markers with an Atheroprotective Immune Response in ApoE() Mice.

Velsko IM, Chukkapalli SS, Rivera-Kweh MF, Chen H, Zheng D, Bhattacharyya I, Gangula PR, Lucas AR, Kesavalu L - PLoS ONE (2015)

Chronic oral infection with F. nucleatum induced significant levels of serum F. nucleatum-specific antibodies.Graphs represent the fold-increase in F. nucleatum-specific IgG or IgM antibody titer in infected mice over control mice at both 12 and 24 weeks of infection. (*** P<0.001).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4469693&req=5

pone.0129795.g002: Chronic oral infection with F. nucleatum induced significant levels of serum F. nucleatum-specific antibodies.Graphs represent the fold-increase in F. nucleatum-specific IgG or IgM antibody titer in infected mice over control mice at both 12 and 24 weeks of infection. (*** P<0.001).
Mentions: Serum antibody response to periodontal pathogens is further evidence of bacterial infection. ELISA antibody analysis of serum samples from 12 week-infected mice showed significantly higher IgG levels in infected mice (approximately 70-fold) than control mice (Fig 2, P = 0.0001). Similarly, IgM antibody levels in 12 week-infected mice were significantly greater (approximately 700-fold) than control mice (P = 0.0001). In addition, IgG levels of 24 week-infected mice were significantly higher (approximately 15-fold) than controls (P = 0.0001), as were IgM levels of 24 week-infected mice (approximately 700-fold) than controls (P = 0.001) (Fig 2).

Bottom Line: The American Heart Association supports an association between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) but does not as of yet support a causal relationship.Chronic oral infection established F. nucleatum colonization in the oral cavity, induced significant humoral IgG (P=0.0001) and IgM (P=0.001) antibody response (12 and 24 weeks), and resulted in significant (P=0.0001) alveolar bone resorption and intrabony defects.Despite evidence for systemic infection in several organs and modulation of known atherosclerosis risk factors, aortic atherosclerotic lesions were significantly reduced after F. nucleatum infection suggesting a potential protective function for this member of the oral microbiota.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontology, College of Dentistry, University of Florida, Gainesville, Florida, United States of America.

ABSTRACT
The American Heart Association supports an association between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) but does not as of yet support a causal relationship. Recently, we have shown that major periodontal pathogens Porphyromonas gingivalis and Treponema denticola are causally associated with acceleration of aortic atherosclerosis in ApoE hyperlipidemic mice. The aim of this study was to determine if oral infection with another significant periodontal pathogen Fusobacterium nucleatum can accelerate aortic inflammation and atherosclerosis in the aortic artery of ApoE mice. ApoE mice (n = 23) were orally infected with F. nucleatum ATCC 49256 and euthanized at 12 and 24 weeks. Periodontal disease assessments including F. nucleatum oral colonization, gingival inflammation, immune response, intrabony defects, and alveolar bone resorption were evaluated. Systemic organs were evaluated for infection, aortic sections were examined for atherosclerosis, and inflammatory markers were measured. Chronic oral infection established F. nucleatum colonization in the oral cavity, induced significant humoral IgG (P=0.0001) and IgM (P=0.001) antibody response (12 and 24 weeks), and resulted in significant (P=0.0001) alveolar bone resorption and intrabony defects. F. nucleatum genomic DNA was detected in systemic organs (heart, aorta, liver, kidney, lung) indicating bacteremia. Aortic atherosclerotic plaque area was measured and showed a local inflammatory infiltrate revealed the presence of F4/80+ macrophages and CD3+ T cells. Vascular inflammation was detected by enhanced systemic cytokines (CD30L, IL-4, IL-12), oxidized LDL and serum amyloid A, as well as altered serum lipid profile (cholesterol, triglycerides, chylomicrons, VLDL, LDL, HDL), in infected mice and altered aortic gene expression in infected mice. Despite evidence for systemic infection in several organs and modulation of known atherosclerosis risk factors, aortic atherosclerotic lesions were significantly reduced after F. nucleatum infection suggesting a potential protective function for this member of the oral microbiota.

No MeSH data available.


Related in: MedlinePlus