Abstract
Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) are Gram-negative anaerobic bacteria possessing several virulence factors that make them potential pathogens associated with periodontal disease. Periodontal diseases are chronic inflammatory diseases of the oral cavity, including gingivitis and periodontitis. Periodontitis can lead to tooth loss and is considered one of the most prevalent diseases worldwide. P. gingivalis and F. nucleatum possess virulence factors that allow them to survive in hostile environments by selectively modulating the host's immune-inflammatory response, thereby creating major challenges to host cell survival. Studies have demonstrated that bacterial infection and the host immune responses are involved in the induction of periodontitis. The NLRP3 inflammasome and its effector molecules (IL-1β and caspase-1) play roles in the development of periodontitis. We and others have reported that the purinergic P2X7 receptor plays a role in the modulation of periodontal disease and intracellular pathogen control. Caspase-4/5 (in humans) and caspase-11 (in mice) are important effectors for combating bacterial pathogens via mediation of cell death and IL-1β release. The exact molecular events of the host's response to these bacteria are not fully understood. Here, we review innate and adaptive immune responses induced by P. gingivalis and F. nucleatum infections and discuss the possibility of manipulations of the immune response as therapeutic strategies. Given the global burden of periodontitis, it is important to develop therapeutic targets for the prophylaxis of periodontopathogen infections.
Highlights
Oral bacteria in dental biofilms contribute to the initiation and progression of periodontal diseases (PD) via exacerbated host inflammatory responses to these bacteria [1, 2]
We demonstrated that the induction of IL-1β mRNA and protein depended on the activation of TLR2 and myeloid differentiation primary response 88 (MyD88) in murine macrophages; the absence of fimbriae did not affect this stimulus (Morandini et al, 2014), it is known that the fimbriae of P. gingivalis activate TLR2, among others, including phosphoceramides and PG1828 lipoprotein [50]
We showed P. gingivalis infection in vivo induced IL-1β production in order to restrain bacterial infection in a manner that was dependent on caspase1/11, P2X7 receptor, and autocrine IL-1 receptor signaling [20]
Summary
Oral bacteria in dental biofilms contribute to the initiation and progression of periodontal diseases (PD) via exacerbated host inflammatory responses to these bacteria [1, 2]. Conventional clinical treatment for periodontitis consists initially of mechanical bacterial removal (scaling and root planning), thereby reducing the contact of bacterial agents with inflammatory and noninflammatory cells in the oral cavity This procedure may not be sufficient to generate clinical improvement. The exact molecular host response events against P. gingivalis and F. nucleatum are not fully understood; understanding of these mechanisms is essential for the identification of therapeutic targets aiming to prevent and treat periodontitis In this context, there are some immunological pathways that have been demonstrated to be involved in the development of periodontitis and in infections with periodontopathogens. Our review highlights the importance of understanding signaling pathways induced by P. gingivalis and F. nucleatum that could potentially serve as effective strategies for treating patients with PD
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