The oral mucosa maintains a functional barrier protecting against chemical, physical, and biological insults. The innate immune response is the first line of defense against pathogens. When the innate immune response detects a danger signal, such as bacteria, tumorigenesis and tissue damage, through the Pathogen Recognition Receptors (PRRs), it initiates an inflammatory response. If this response is not regulated, it can lead to an uncontrolled inflammation, septic shock, cancer or autoimmune diseases. Several mechanisms, including epigenetic changes, have been suggested to influence the downstream signaling from epithelial cells to inflammatory cells in the connective tissue thereby further regulating the inflammatory processes not only in the innate immune response but also the adapted immune response. Chronic inflammation and/or abrupt microbial imbalance (dysbiosis) dynamically alter cellular and molecular events, leading to the development of disease such as inflammatory bowel disease, irritable bowel syndrome, celiac disease, colitis, and periodontitis among other diseases.
The goal of this Research Topic is, by using a broad perspective, linking events in epithelial cells with those of cells in the connective tissue in order to give a better understanding on how the signaling initiated by the recognition of bacteria by receptors in the epithelium is transferred to the underlying tissue and further promote an immune response.
An additional goal is to discuss how changes in these signaling pathways can contribute to chronic inflammation, endotoxin tolerance and tumorigenesis.
Original Research articles as well as Reviews focusing on the following sub-themes are welcome:
• Bacterial interaction with the immune response
• The role of epithelium in bacterial recognition
• The consequence of bacterial activation of epithelial cells on connective tissue
• Endotoxin tolerance
• The role of epigenetic on bacterial recognition and immune response
The oral mucosa maintains a functional barrier protecting against chemical, physical, and biological insults. The innate immune response is the first line of defense against pathogens. When the innate immune response detects a danger signal, such as bacteria, tumorigenesis and tissue damage, through the Pathogen Recognition Receptors (PRRs), it initiates an inflammatory response. If this response is not regulated, it can lead to an uncontrolled inflammation, septic shock, cancer or autoimmune diseases. Several mechanisms, including epigenetic changes, have been suggested to influence the downstream signaling from epithelial cells to inflammatory cells in the connective tissue thereby further regulating the inflammatory processes not only in the innate immune response but also the adapted immune response. Chronic inflammation and/or abrupt microbial imbalance (dysbiosis) dynamically alter cellular and molecular events, leading to the development of disease such as inflammatory bowel disease, irritable bowel syndrome, celiac disease, colitis, and periodontitis among other diseases.
The goal of this Research Topic is, by using a broad perspective, linking events in epithelial cells with those of cells in the connective tissue in order to give a better understanding on how the signaling initiated by the recognition of bacteria by receptors in the epithelium is transferred to the underlying tissue and further promote an immune response.
An additional goal is to discuss how changes in these signaling pathways can contribute to chronic inflammation, endotoxin tolerance and tumorigenesis.
Original Research articles as well as Reviews focusing on the following sub-themes are welcome:
• Bacterial interaction with the immune response
• The role of epithelium in bacterial recognition
• The consequence of bacterial activation of epithelial cells on connective tissue
• Endotoxin tolerance
• The role of epigenetic on bacterial recognition and immune response
