Porphyromonas gingivalis (P. gingivalis), formerly known as Bacteroides gingivalis, is a gram-negative, asaccharolytic, obligate, capnocytophagic, anaerobic, rod-shaped oral bacteria, primarily associated with the pathogenesis and progression of periodontitis. Recently, P. gingivalis has been referred to as a ‘keystone pathogen’ and a ‘master of polymicrobial synergy, dysbiosis and immune subversion’, as it can engineer its environment or modify its nutritional demands, virulence factors, and its interaction with other bacteria in the biofilm to survive in the host. It can even exploit several sabotage tactics to evade, weaken, or deceive the host’s immune system and enter the systemic circulation.
P. gingivalis invasion into the systemic circulation affects various signaling pathways and cells of inflammation, oxidative stress, acute phase response, complement system, apoptosis, immune response, and cell-cycle. It’s even known to induce the suicidal cell death of the host cells and other microbes in its vicinity along with the development of many pathobiont species. Due to its ability to deceive the host immune response and cellular invasion properties, P. gingivalis has been linked with various systemic diseases like rheumatoid arthritis, Alzheimer’s disease, adverse pregnancy outcomes, stroke, and cardiovascular disease. It has also been linked with the development of various precancerous and cancerous lesions. Hence this Research Topic is dedicated to exploring the intricate and unique molecular mechanisms by which P. gingivalis can evade the host immune response, survive within the host, and induces dysbiosis and various organ dysfunctions.
This Research Topics welcomes Original Research articles, Reviews, Mini reviews, and Commentaries that provide recent breakthroughs in pathogenic mechanisms, virulence factors, pathways, and interactions of this obligate keystone pathogen with its host. We are particularly interested in the following sub-topics:
• Novel virulence factors and strategic mechanisms of P. gingivalis linked with onset of dysbiosis in the host, cellular invasion, survival, persistence, immune evasion, and cellular dysfunction.
• Mechanisms by which P. gingivalis interacts with its hosts: specific cells, receptors, signaling pathways, other microorganisms and molecules in the host.
• Pathways and alterations in host cell function by P. gingivalis and how it can relate to both health and disease in the host.
• Studies evaluating the mode of infection, colonization and interaction of P. gingivalis with other microorganisms/microbiome in the host.
• Pathogenic mechanisms explaining how P. gingivalis can induce dysbiosis, exaggerated inflammation, oxidative stress and organ dysfunction. Effect of P. gingivalis on specific proteins, molecules, and biomarkers of systemic circulation.
• Studies on P. gingivalis as risk factor for initiating or worsening diseases related to cardiovascular, renal, reproductive (pregnancy and fetal health), digestive (gut), endocrine (diabetes), and nervous systems (Alzheimer's disease), and P. gingivalis as a risk factor for precancerous and cancer lesion in the host.
Porphyromonas gingivalis (P. gingivalis), formerly known as Bacteroides gingivalis, is a gram-negative, asaccharolytic, obligate, capnocytophagic, anaerobic, rod-shaped oral bacteria, primarily associated with the pathogenesis and progression of periodontitis. Recently, P. gingivalis has been referred to as a ‘keystone pathogen’ and a ‘master of polymicrobial synergy, dysbiosis and immune subversion’, as it can engineer its environment or modify its nutritional demands, virulence factors, and its interaction with other bacteria in the biofilm to survive in the host. It can even exploit several sabotage tactics to evade, weaken, or deceive the host’s immune system and enter the systemic circulation.
P. gingivalis invasion into the systemic circulation affects various signaling pathways and cells of inflammation, oxidative stress, acute phase response, complement system, apoptosis, immune response, and cell-cycle. It’s even known to induce the suicidal cell death of the host cells and other microbes in its vicinity along with the development of many pathobiont species. Due to its ability to deceive the host immune response and cellular invasion properties, P. gingivalis has been linked with various systemic diseases like rheumatoid arthritis, Alzheimer’s disease, adverse pregnancy outcomes, stroke, and cardiovascular disease. It has also been linked with the development of various precancerous and cancerous lesions. Hence this Research Topic is dedicated to exploring the intricate and unique molecular mechanisms by which P. gingivalis can evade the host immune response, survive within the host, and induces dysbiosis and various organ dysfunctions.
This Research Topics welcomes Original Research articles, Reviews, Mini reviews, and Commentaries that provide recent breakthroughs in pathogenic mechanisms, virulence factors, pathways, and interactions of this obligate keystone pathogen with its host. We are particularly interested in the following sub-topics:
• Novel virulence factors and strategic mechanisms of P. gingivalis linked with onset of dysbiosis in the host, cellular invasion, survival, persistence, immune evasion, and cellular dysfunction.
• Mechanisms by which P. gingivalis interacts with its hosts: specific cells, receptors, signaling pathways, other microorganisms and molecules in the host.
• Pathways and alterations in host cell function by P. gingivalis and how it can relate to both health and disease in the host.
• Studies evaluating the mode of infection, colonization and interaction of P. gingivalis with other microorganisms/microbiome in the host.
• Pathogenic mechanisms explaining how P. gingivalis can induce dysbiosis, exaggerated inflammation, oxidative stress and organ dysfunction. Effect of P. gingivalis on specific proteins, molecules, and biomarkers of systemic circulation.
• Studies on P. gingivalis as risk factor for initiating or worsening diseases related to cardiovascular, renal, reproductive (pregnancy and fetal health), digestive (gut), endocrine (diabetes), and nervous systems (Alzheimer's disease), and P. gingivalis as a risk factor for precancerous and cancer lesion in the host.