Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.

Immunology and cell biology - 1 Sept 2015

Lam Roselind S, O'Brien-Simpson Neil M, Hamilton John A, Lenzo Jason C, Holden James A, Brammar Gail C, Orth Rebecca K, Tan Yan, Walsh Katrina A, Fleetwood Andrew J, Reynolds Eric C

Abstract excerpt

Granulocyte-macrophage colony-stimulating factor (GM-CSF) and urokinase-type plasminogen activator (uPA) can contribute to the progression of chronic inflammatory diseases with possible involvement of macrophages. In this study, we investigated the role of both GM-CSF and uPA in Porphyromonas gingivalis-induced experimental periodontitis using GM-CSF-/- and uPA-/- mice. Intra-oral inoculation of wild-type (WT)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alveolar Bone Loss
Share to Dental Plaque

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Granulocyte-Macrophage Colony-Stimulating Factor

Share to Macrophages, Peritoneal

Share to Periodontitis

Share to Porphyromonas gingivalis

Share to T-Cell Antigen Receptor Specificity

Share to Urokinase-Type Plasminogen Activator

Source

Identifiers

PMID: 25753270
DOI: 10.1038/icb.2015.25

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.PMID 25753270Read ↗

Evaluation of the Host Response in Various Models of Induced Periodontal Disease in MiceSemantic proximity Read ↗

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis.Semantic proximity Read ↗

The interleukin-10 knockout mouse is highly susceptible to Porphyromonas gingivalis-induced alveolar bone loss.Semantic proximity Read ↗

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences.Semantic proximity Read ↗

T cell response mediated by myeloid cell-derived IL-12 is responsible for Porphyromonas gingivalis-induced periodontitis in IL-10-deficient mice.Semantic proximity Read ↗

RANK/RANKL/OPG Signalization Implication in Periodontitis: New Evidence from a RANK Transgenic Mouse ModelSemantic proximity Read ↗

Enhanced monocyte migration and pro-inflammatory cytokine production by Porphyromonas gingivalis infection.Semantic proximity Read ↗

Streptococcus cristatus ArcA interferes with Porphyromonas gingivalis pathogenicity in mice.Semantic proximity Read ↗

Genetic control of susceptibility to Porphyromonas gingivalis-induced alveolar bone loss in mice.Semantic proximity Read ↗

Antibody responses to Porphyromonas gingivalis infection in a murine abscess model--involvement of gingipains and responses to re-infection.Semantic proximity Read ↗

Disruption of granulocyte macrophage-colony stimulating factor production in the lungs severely affects the ability of mice to control Mycobacterium tuberculosis infection.Semantic proximity Read ↗

Porphyromonas gingivalis fimbriae are pro-inflammatory but do not play a prominent role in the innate immune response to P. gingivalis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.