Disruption of epithelial barrier and impairment of cellular function by Porphyromonas gingivalis

Abstract

Porphyromonas gingivalis is a predominant periodontal pathogen that expresses a number of potential virulence factors involved in the pathogenesis of periodontitis. Gingival epithelial cells are spontaneously exposed to bacterial attacks and function to prevent invasion by bacteria into deeper tissues. P. gingivalis fimbriae are a critical factor for mediation of interaction of the organism with host tissues, as they promote both bacterial adhesion to and invasion of targeted sites. Fimbriae are capable of binding to human salivary components, extracellular matrix proteins, and commensal bacteria, while they also strongly adhere to cellular alpha5beta1-integrin. Following adhesion to alpha5beta1-integrin, P. gingivalis is captured by cellular pseudopodia, which enables invagination through an actin-mediated pathway. The invasive event has been reported to require host cellular dynamin, actin fibers, microtubules, and lipid rafts. Following passage through the epithelial barrier, the intracellular pathogen impairs cellular function. Fimbriae are classified into 6 genotypes (types I to V and Ib) based on the diversity of the fimA genes encoding each fimbria subunit, and intracellular P. gingivalis with type II fimbriae has been found to clearly degrade integrin-related signaling molecules, paxillin, and focal adhesion kinase, which disables cellular migration and proliferation. These events are considered to integrate the bacterial strategy for persistence in periodontal tissues.