Evidence map›Paper›PMID 24126519›Full record

ArticleInfection and immunity2014

Secondary lymphoid organ homing phenotype of human myeloid dendritic cells disrupted by an intracellular oral pathogen.

Brodie Miles, Ibrahim Zakhary, Ahmed El-Awady, Elizabeth Scisci, Julio Carrion, John C O'Neill, Aaron Rawlings, J Kobi Stern, Cristiano Susin, Christopher W Cutler

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 32 citations in OpenAlex.

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  8. Frontiers in immunology · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Brodie MilesDepartment of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA.
Ibrahim Zakhary
Ahmed El-Awady
Elizabeth Scisci
Julio Carrion
John C O'Neill
Aaron Rawlings
J Kobi Stern
Cristiano Susin
Christopher W Cutler
Augusta University · USGeorgia Regents Medical Center · USStony Brook School · USStony Brook University · US

Funding

Oral Pathogens and Dendritic Cell SubsetsR01DE014328 · NIDCR · STATE UNIVERSITY NEW YORK STONY BROOK · PI CUTLER, CHRISTOPHER WILLIAM · 2001 to 2014
$5.1M
Dendritic Cells Trafficking in Gingival Health and DiseaseK23DE018187 · NIDCR · STATE UNIVERSITY NEW YORK STONY BROOK · PI CARRION, JULIO A. · 2007 to 2011
$540k
DENDRITIC CELLS, LPS AND ORAL MUCOSAR21DE014160 · NIDCR · STATE UNIVERSITY NEW YORK STONY BROOK · PI CUTLER, CHRISTOPHER W · 2000 to 2001
$388k
Peripheral blood dendritic cells and periodontitisR21DE020916 · NIDCR · STATE UNIVERSITY NEW YORK STONY BROOK · PI CUTLER, CHRISTOPHER WILLIAM · 2011 to 2012
$362k
Neutrophil and Dendritic Cell InteractionsF30DE021649 · NIDCR · STATE UNIVERSITY NEW YORK STONY BROOK · PI SCISCI, ELIZABETH · 2011 to 2015
$181k
NIDCR NIH HHS F30 DE021649NIDCR NIH HHS F30 DE021649-01NIDCR NIH HHS K23 DE018187NIDCR NIH HHS R01 DE014328NIDCR NIH HHS R21 DE020916
6 · The paper itself

Abstract

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 monocyte-derived 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.

Indexed as

Bacteroidaceae InfectionsCase-Control StudiesCell Adhesion MoleculesCell MovementChemokine CXCL12ChemotaxisChronic PeriodontitisDC-Specific ICAM-3 Grabbing NonintegrinDendritic CellsEndothelial CellsFimbriae, BacterialHumansLectins, C-TypeLipopolysaccharidesMyeloid CellsNeovascularization, PathologicCCR7 protein, humanCell Adhesion MoleculesChemokine CXCL12CXCL12 protein, humanDC-Specific ICAM-3 Grabbing NonintegrinLectins, C-TypeLipopolysaccharidesReceptors, CCR7Receptors, Cell SurfaceReceptors, ChemokineReceptors, CXCR4Tumor Necrosis Factor-alpha

Identifiers

PMID24126519
PMCPMC3911834
OpenAlexW2158930967

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.