The mucosal barrier of the host is composed of the epithelium lining, underneath immune cells, as well as the inflammation responses and secreted pro-inflammatory molecules in-between. Most pathogens, especially the food/water/air-borne germs, would have to interact with the mucosal barrier system in order to invade hosts.
Intracellular pathogens such as microsporidia, Mycobacterium tuberculosis, salmonella and so many on can cause both acute as well as chronic infections. We are very interested in the pathogenesis of these intracellular pathogens and how they interact with a mucosal barrier. In particular, how the commensal flora is disrupted by the invading pathogens? How the local immune tolerance is interrupted? How the epithelium function as a sentinel barrier to detect and respond to pathogens? How the residential immune cells such as macrophages and dendritic cells are stimulated? How the pro-inflammatory signaling pathways are up-regulated in the process? Etc. Notably that the armed race between the immune response and the pathogens is also of great importance. For example, how the pathogens develop strategies to evade the hosts’ immune responses.
This Research Topic will give a comprehensive overview of the interactions between intracellular pathogens with mucosal barrier especially the epithelium and underneath immune cells. In this Research Topic, we welcome studies on both vertebrate and invertebrate intracellular pathogens focusing on interactions with a mucosal barrier. We seek Original Research Articles, Reviews, Brief Research Reports, and Mini-Reviews that cover, but are not limited to, the following topics:
• Role of the mucosal lining (epithelium/endothelium) in pathogen recognition, immune response initiation and pathogen dissemination
• Functions of residential innate immune cells during the course
• Molecular mechanisms/Signaling pathways that are essential during infections
• Roles of mucosal barrier to the disease outcome, such as the balance between pathogen clearance, acute infection, and chronic inflammation
The mucosal barrier of the host is composed of the epithelium lining, underneath immune cells, as well as the inflammation responses and secreted pro-inflammatory molecules in-between. Most pathogens, especially the food/water/air-borne germs, would have to interact with the mucosal barrier system in order to invade hosts.
Intracellular pathogens such as microsporidia, Mycobacterium tuberculosis, salmonella and so many on can cause both acute as well as chronic infections. We are very interested in the pathogenesis of these intracellular pathogens and how they interact with a mucosal barrier. In particular, how the commensal flora is disrupted by the invading pathogens? How the local immune tolerance is interrupted? How the epithelium function as a sentinel barrier to detect and respond to pathogens? How the residential immune cells such as macrophages and dendritic cells are stimulated? How the pro-inflammatory signaling pathways are up-regulated in the process? Etc. Notably that the armed race between the immune response and the pathogens is also of great importance. For example, how the pathogens develop strategies to evade the hosts’ immune responses.
This Research Topic will give a comprehensive overview of the interactions between intracellular pathogens with mucosal barrier especially the epithelium and underneath immune cells. In this Research Topic, we welcome studies on both vertebrate and invertebrate intracellular pathogens focusing on interactions with a mucosal barrier. We seek Original Research Articles, Reviews, Brief Research Reports, and Mini-Reviews that cover, but are not limited to, the following topics:
• Role of the mucosal lining (epithelium/endothelium) in pathogen recognition, immune response initiation and pathogen dissemination
• Functions of residential innate immune cells during the course
• Molecular mechanisms/Signaling pathways that are essential during infections
• Roles of mucosal barrier to the disease outcome, such as the balance between pathogen clearance, acute infection, and chronic inflammation