![]() The FimBCDE proteins are not well characterized, but FimCDE appear to be minor structural components of the fimbria involved in adhesion specificity, and FimB, although not essential for fimbria assembly, is involved in regulation of fimbrial length –. gingivalis are primarily composed of the structural protein subunit FimA, encoded by the fimA gene, additional components are encoded by downstream genes fimB, fimC, fimD, and fimE. Major fimbriae also interact with TLR2 receptors, cross-linking them with CXCR4 to block receptor signaling, making fimbriae mechanistically important for key events in immune dysregulation. gingivalis into the host cell, localized suppression of cytokine production, inhibition of apoptotic signaling pathways, and interference with cell differentiation and mineralization –. Beta-1 integrin has been identified as the host receptor on multiple cell types binding of integrin by the major fimbriae activates a cascade of events that result in internalization of P. The major fimbriae are multifunctional adhesins, and mediate adherence to and signaling within bacterial biofilms and host tissues. gingivalis colonization and survival in the host are attributable to a number of persistence factors, including biofilm formation, production of capsule, secretion of proteases, and the presence of major and minor fimbriae. gingivalis: creation of the periodontal pocket, an enlarged sub-gingival space that provides ideal conditions for propagation of this strictly anaerobic, proteolytic microbe. The outcome of tissue destruction is beneficial to P. gingivalis and other opportunistic pathogens within the oral flora to overcome mucosal defenses and stimulate the inflammatory destruction of the periodontal connective tissues. Inhibition of these host defenses results in a significant increase in total bacterial burden in the sub-gingival sulcus, and enables P. The most important immune dysregulation events appear to be inhibition of IL-8 secretion, subversion of the complement system, and Toll-like receptor antagonism. gingivalis has multiple strategies for undermining the long-term effectiveness of host defenses, and has been shown in a recent landmark study to be a “keystone” pathogen, able to disrupt host-microbe homeostasis by molecular manipulation of select host protective mechanisms. gingivalis and co-resident commensal microorganisms in close proximity to the non-keratinized junctional epithelium, and in a healthy periodontium, the bacterial burden is restricted by circulating neutrophils and innate immune effectors. Residence within sub-gingival biofilms places P. This bacterium colonizes established multi-species plaque biofilms at the gingival margin and in the sub-gingival sulcus –. Porphyromonas gingivalis is a gram-negative anaerobe that preferentially inhabits the human oral cavity and is a key etiologic agent in the development of periodontal disease. Understanding how these opportunistic bacteria shift from commensal to pathogenic in the host environment will prove pivotal in combating these resourceful organisms in the future. Typically this adaptation process is thought to be driven by spontaneous mutation and horizontal DNA transfer events with the increasing availability of strain-level genome sequences, identification and molecular characterization of these adaptive virulence events is becoming possible. ![]() Further subdividing the opportunistic pathogens, there are a few species that colonize as part of the normal flora, but may evolve within the host habitat to adopt a more overtly pathogenic phenotype. Within these thousands of species are many that are also opportunistic pathogens, capable of causing disease in the event of a failure of host defenses. ![]() Complex communities of commensal microorganisms comprise the vast majority of the human body’s natural flora.
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