Abstract
The oral microbiome, one of the most complex and intensive microbial ecosystems in the human body, comprises bacteria, archaea, fungi, protozoa, and viruses. Dysbiosis of the oral microbiome is the initiating factor that leads to oral infectious diseases. Infection is a sophisticated biological process involving interplay between the pathogen and the host, which often leads to activation of programmed cell death. Studies suggest that pyroptosis, apoptosis, and necroptosis are involved in multiple oral infectious diseases. Further understanding of crosstalk between cell death pathways has led to pyroptosis, apoptosis, and necroptosis being integrated into a single term: PANoptosis. PANoptosis is a multifaceted agent of the immune response that has important pathophysiological relevance to infectious diseases, autoimmunity, and cancer. As such, it plays an important role in innate immune cells that detect and eliminate intracellular pathogens. In addition to the classical model of influenza virus-infected and Yersinia-infected macrophages, other studies have expanded the scope of PANoptosis to include other microorganisms, as well as potential roles in cell types other than macrophages. In this review, we will summarize the pathophysiological mechanisms underlying inflammation and tissue destruction caused by oral pathogens. We present an overview of different pathogens that may induce activation of PANoptosis, along with the functional consequences of PANoptosis in the context of oral infectious diseases. To advance our understanding of immunology, we also explore the strategies used by microbes that enable immune evasion and replication within host cells. Improved understanding of the interplay between the host and pathogen through PANoptosis will direct development of therapeutic strategies that target oral infectious diseases.
Highlights
The oral microbiome is the general term used to describe the bacteria, fungi, and viruses that colonize the oral cavity
These findings consistently demonstrated that regulation of PANoptosis by RIPK1 is essential for homeostasis, cell death, and inflammation through kinasedependent and -independent functions
When the NLRP3 inflammasome was downregulated using siRNAs, cells were protected from apoptotic and pyroptic death [77]. These results indicate that NLRP3 is involved in apoptosis and pyroptosis of MG63 cells
Summary
The oral microbiome is the general term used to describe the bacteria, fungi, and viruses that colonize the oral cavity. With the enormous progress in understanding the pathogenesis of oral infectious diseases, cell death is considered to be the vital mechanism for host defense and inflammationmediated immune response. More comprehensive understanding of pathogen-induced cell death provides underlying therapeutic targets for blocking uncontrolled inflammation, and deliver new insights into the prevention and treatment for oral infectious diseases in clinical setting. Infection by oral pathogens activates caspases and other effector molecules, resulting in cell death and cytokines release. Emerging and ongoing efforts have revealed many links between PANoptosis and oral infectious diseases, and integrating and summarizing these evidence can advance our understanding of the role of PANoptosis in oral infectious diseases, helping to uncover the complex network which existed among multiple molecular events of the host’s response to those pathogens. We discuss the possibility of manipulating the immune response as a therapeutic strategy, as well as the search for potential molecular targets for treatment and prevention
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
