Porphyromonas gingivalis mediates the shedding and proteolysis of complement regulatory protein CD46 expressed by

Related Experiment Video

Updated: Jun 20, 2026

Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
12:16

Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

Published on: December 17, 2015

H Mahtout1, F Chandad, J M Rojo

  • 1Groupe de Recherche en Ecologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, QC, Canada.

Oral Microbiology and Immunology
|August 26, 2009
PubMed
Abstract

Insights

Porphyromonas gingivalis, a key cause of periodontitis, triggers the shedding and breakdown of CD46 on oral cells. This process may increase susceptibility to complement-mediated damage and inflammation in periodontitis.

Area of Science:

  • Oral microbiology
  • Immunology
  • Complement system

Background:

  • Human cells utilize membrane-bound complement regulatory proteins to prevent self-damage.
  • Porphyromonas gingivalis is a primary etiological agent of chronic periodontitis.

Purpose of the Study:

  • To investigate if Porphyromonas gingivalis induces shedding or proteolysis of CD46 on oral epithelial cells.
  • To determine the role of CD46 in P. gingivalis-induced inflammation.

Main Methods:

  • Oral epithelial cells were exposed to P. gingivalis culture.
  • CD46 levels (membrane-bound and shed) were measured using ELISA.
  • Proteolytic degradation of CD46 by P. gingivalis was analyzed via SDS-PAGE/Western immunoblotting.

Main Results:

  • P. gingivalis treatment led to increased shed CD46 in conditioned media.
  • Soluble CD46 stimulated dose-dependent IL-8 secretion from epithelial cells.
  • P. gingivalis and its Lys-gingipain degraded CD46 in a dose-dependent manner.

Conclusions:

  • P. gingivalis induces CD46 shedding/proteolysis from oral epithelial cells.
  • This mechanism may increase host cell susceptibility to complement-mediated damage.
  • The findings suggest a role in periodontitis-related tissue damage and inflammation.

More Related Videos

Organotypic Tissue Model Systems for Investigating Host-Pathogen Interactions In Vitro08:41

Organotypic Tissue Model Systems for Investigating Host-Pathogen Interactions In Vitro

Published on: March 28, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Related Concept Videos

The Oral Microbiota01:27

The Oral Microbiota

The oral microbiome includes a complex ecosystem comprising over 700 microbial species, identified through genomic sequencing and culture-based analyses to date. This community includes a core microbiome, found universally among individuals, and a variable component influenced by environmental factors such as diet, lifestyle, and host genetics. Site-specific conditions, including oxygen gradients, pH levels, and nutrient availability, determine the spatial distribution of these microorganisms...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Formation of Lipopolysaccharides01:19

Formation of Lipopolysaccharides

Lipopolysaccharides (LPS) are crucial components of the outer membrane of Gram-negative bacteria, serving both structural and functional roles. It contributes to membrane stability and protects bacteria from host immune responses. LPS is composed of three major regions—lipid A, a core oligosaccharide, and an O antigen. The biosynthesis and assembly of LPS involve a highly coordinated set of enzymatic reactions and transport mechanisms. Additionally, LPS is recognized as an endotoxin, triggering...
Development of the Oral Microbiota01:28

Development of the Oral Microbiota

The establishment of the oral microbiome begins before birth, challenging the long-held belief that the fetal oral cavity is sterile. The presence of oral microbes such as Streptococcus and Fusobacterium in amniotic fluid suggests that microbial exposure may occur in utero, potentially through translocation from the maternal oral or gastrointestinal tract. This early colonization primes the neonatal immune system and sets the stage for subsequent microbial succession. Maternal health,...