Microbial Carriage State of Peripheral Blood Dendritic Cells (DCs) in Chronic Periodontitis Influences DC Differentiation, Atherogenic Potential

Carrion, Julio; Scisci, Elizabeth; Brodie, MJ; Sabino, Gregory J.; Zeituni, Amir E.; Gu, Ying; Bear, Adam; Genco, Caroline Attardo; Brown, David L.; Cutler, Christopher W.

doi:10.4049/jimmunol.1201053

Cited by 135 publications

(172 citation statements)

References 78 publications

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“…Moreover, sera from chronic periodontitis subjects express elevated levels of CXCR4 ligand CXCL12 compared to those of healthy controls. These data, combined with our previously published evidence for P. gingivalis dissemination within mDCs to coronary artery plaques (22), provide a mechanistic framework for how this intracellular pathogen directs its dissemination in DCs in vivo.…”

mentioning

confidence: 82%

“…Protocols for healthy mDC and sera were approved by the Committee on Research Involving Human Subjects (CORIHS) at Stony Brook University. The study population and demographics have been previously outlined (22).…”

Section: Methodsmentioning

confidence: 99%

“…This is particularly pertinent in view of evidence that P. gingivalis disseminates from its oral mucosal niche to distant sites, such as the respiratory tract (25), atherosclerotic plaques (26,27), arthritic lesions (28), and the gut (29). We have shown that blood mDCs disseminate P. gingivalis to atherosclerotic plaques (22), but the mechanisms are not clear.…”

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confidence: 99%

“…Our group has previously reported that P. gingivalis takes advantage of these DC characteristics by infecting DCs and being routed into a protective niche that shields P. gingivalis from more-efficient extracellular killing (22). Optimal infection of DCs by P. gingivalis is dependent on its glycosylated minor (mfa-1) fimbrial adhesin, which targets the c-type lectin dendritic cell specific ICAM-3 grabbing nonintegrin (DC-SIGN) for entry (23).…”

mentioning

confidence: 99%

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Secondary Lymphoid Organ Homing Phenotype of Human Myeloid Dendritic Cells Disrupted by an Intracellular Oral Pathogen

et al. 2014

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c Several intracellular pathogens, including a key etiological agent of chronic periodontitis, Porphyromonas gingivalis, infect blood myeloid dendritic cells (mDCs). This infection results in pathogen dissemination to distant inflammatory sites (i.e., pathogen trafficking). The alteration in chemokine-chemokine receptor expression that contributes to this pathogen trafficking function, particularly toward sites of neovascularization in humans, is unclear. To investigate this, we utilized human monocytederived DCs (MoDCs) and primary endothelial cells in vitro, combined with ex vivo-isolated blood mDCs and serum from chronic periodontitis subjects and healthy controls. Our results, using conditional fimbria mutants of P. gingivalis, show that P. gingivalis infection of MoDCs induces an angiogenic migratory profile. This profile is enhanced by expression of DC-SIGN on MoDCs and minor mfa-1 fimbriae on P. gingivalis and is evidenced by robust upregulation of CXCR4, but not secondary lymphoid organ (SLO)-homing CCR7. This disruption of SLO-homing capacity in response to respective chemokines closely matches surface expression of CXCR4 and CCR7 and is consistent with directed MoDC migration through an endothelial monolayer. Ex vivo-isolated mDCs from the blood of chronic periodontitis subjects, but not healthy controls, expressed a similar migratory profile; moreover, sera from chronic periodontitis subjects expressed elevated levels of CXCL12. Overall, we conclude that P. gingivalis actively "commandeers" DCs by reprogramming the chemokine receptor profile, thus disrupting SLO homing, while driving migration toward inflammatory vascular sites.

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confidence: 82%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Secondary Lymphoid Organ Homing Phenotype of Human Myeloid Dendritic Cells Disrupted by an Intracellular Oral Pathogen

et al. 2014

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“…At the same time, Carrion et al demonstrated that blood myeloid DCs play a role in harboring and disseminating oral pathogens to atheromatous plaques, suggesting also a direct effect of bacterial contamination in the determination of atherosclerotic lesions. 11 In the Oral Infection and Vascular Disease Epidemiology Study, 4,561 biofilm samples were collected from 593 patients for the assessment of bacterial species and found significantly increased levels of secretory phospholipase A2 and lipoprotein-associated PLA2, two inflammatory enzymes associated with atherosclerosis. 12 At the same time, Mahendra et al proved that patients with cardiovascular diseases (CVD) exhibit higher levels of periodontal pathogens in subgingival biofilms, and that the amount of subgingival bacteria was significantly associated with the amount of bacteria identified in the atherosclerotic plaques.…”

Section: Inflammation -A Common Pathway For Periodontal Disease and Amentioning

confidence: 99%

Review. The Link between Periodontal Disease, Inflammation and Atherosclerosis — an Interdisciplinary Approach

Benedek

2017

Journal of Interdisciplinary Medicine

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Periodontal disease is a chronic inflammatory disease that results from the activity of altered oral microbiome, leading to altered immune reaction, destruction of tissues supporting the teeth, and oral bone loss. This disease is particularly associated with an expressed systemic inflammation, being considered nowadays an inflammatory disorder. At the same time, inflammation has been recognized to play a major role in the development of atherosclerotic lesions. Atheromatous plaque formation is triggered by alterations in the structure of the endothelium, which lead to the expression of adhesion molecules and recruitment of immune cells such as macrophages, in the arterial wall. While the association between periodontal disease, inflammation and cardiovascular diseases has been well established, the causality relation between these three entities has not been demonstrated so far. This review presents the most common advances in understanding the complex link between periodontal disease, inflammation and atherosclerosis, as a common pathway leading to increased cardiovascular risk.

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Parvimonas micra can translocate from the subgingival sulcus of the human oral cavity to colorectal adenocarcinoma

Conde‐Pérez,

Buetas,

Aja‐Macaya

et al. 2023

Molecular Oncology

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Oral and intestinal samples from a cohort of 93 colorectal cancer (CRC) patients and 30 healthy controls (non‐CRC) were collected for microbiome analysis. Saliva (28 non‐CRC and 94 CRC), feces (30 non‐CRC and 97 CRC), subgingival fluid (20 CRC) and tumor tissue samples (20 CRC) were used for 16S metabarcoding and/or RNA sequencing (RNAseq) approaches. A differential analysis of the abundance, performed with the ANCOM‐BC package, adjusting the p‐values by the Holm‐Bonferroni method, revealed that Parvimonas was significantly over‐represented in feces from CRC patients (p‐value <0.001) compared to healthy controls. A total of 11 Parvimonas micra isolates were obtained from the oral cavity and adenocarcinoma of CRC patients. Genome analysis identified a pair of isolates from the same patient that shared 99.2% identity, demonstrating that P. micra can translocate from the subgingival cavity to the gut. The data suggest that P. micra could migrate in a synergistic consortium with other periodontal bacteria. Metatranscriptomics confirmed that oral bacteria were more active in tumor than in non‐neoplastic tissues. We suggest that P. micra could be considered as a CRC biomarker detected in non‐invasive samples such as feces.

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Microbial Carriage State of Peripheral Blood Dendritic Cells (DCs) in Chronic Periodontitis Influences DC Differentiation, Atherogenic Potential

Cited by 135 publications

References 78 publications

Secondary Lymphoid Organ Homing Phenotype of Human Myeloid Dendritic Cells Disrupted by an Intracellular Oral Pathogen

Secondary Lymphoid Organ Homing Phenotype of Human Myeloid Dendritic Cells Disrupted by an Intracellular Oral Pathogen

Review. The Link between Periodontal Disease, Inflammation and Atherosclerosis — an Interdisciplinary Approach

Parvimonas micra can translocate from the subgingival sulcus of the human oral cavity to colorectal adenocarcinoma

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