The intestinal epithelium provides a physical barrier that separates the many trillions of intestinal microbiota (commensal and pathogenic) in the intestinal lumen from the underlying lamina propria and the deeper intestinal layers. Defective intestinal epithelial tight junction (TJ) barrier, characterized by an increase in intestinal permeability, has been shown to be an important factor contributing to the pathogenicity of some enteric bacteria. It has been demonstrated that some enteric pathogens can induce permeability defects in gut epithelia, mediated by their virulence proteins or toxins, by allowing paracellular translocation of pathogen or permeation of luminal antigens that elicit and promote inflammatory response.
Understanding the complex interaction between intestinal microbiota (commensal and pathogenic) and the host intestinal epithelial TJ barrier may provide crucial insights into the pathogenesis of gut inflammation as well as interventions to prevent intestinal epithelial barrier dysfunction and subsequently reduce the development of intestinal inflammation.
This Research Topic welcomes Original research and Review articles in the field, with a focus on but not limited to:
• The molecular basis for enteric pathogens modulation of intestinal barrier function, regulation of host physiology and cellular function;
• In vitro and in vivo model systems for enteric pathogenesis, signaling pathways induced by innate immune receptors demonstrating the active role of intestinal epithelial TJ barrier in the host-microbial interplay;
• Clinical research on the mucosal interaction between host and microbes contributing to development in intestinal and systemic inflammation;
• Studies investigating interventions or solutions to eliminate enteric pathogens, strengthen epithelial barrier function, or block enteric pathogens-induced intestinal inflammation are encouraged.
Topic Editor Arun K. Bhunia receives financial support from BioMatrix International and United Animal Health and holds patents. The other Topic Editor declares no competing interests with regard to the Research Topic subject.
The intestinal epithelium provides a physical barrier that separates the many trillions of intestinal microbiota (commensal and pathogenic) in the intestinal lumen from the underlying lamina propria and the deeper intestinal layers. Defective intestinal epithelial tight junction (TJ) barrier, characterized by an increase in intestinal permeability, has been shown to be an important factor contributing to the pathogenicity of some enteric bacteria. It has been demonstrated that some enteric pathogens can induce permeability defects in gut epithelia, mediated by their virulence proteins or toxins, by allowing paracellular translocation of pathogen or permeation of luminal antigens that elicit and promote inflammatory response.
Understanding the complex interaction between intestinal microbiota (commensal and pathogenic) and the host intestinal epithelial TJ barrier may provide crucial insights into the pathogenesis of gut inflammation as well as interventions to prevent intestinal epithelial barrier dysfunction and subsequently reduce the development of intestinal inflammation.
This Research Topic welcomes Original research and Review articles in the field, with a focus on but not limited to:
• The molecular basis for enteric pathogens modulation of intestinal barrier function, regulation of host physiology and cellular function;
• In vitro and in vivo model systems for enteric pathogenesis, signaling pathways induced by innate immune receptors demonstrating the active role of intestinal epithelial TJ barrier in the host-microbial interplay;
• Clinical research on the mucosal interaction between host and microbes contributing to development in intestinal and systemic inflammation;
• Studies investigating interventions or solutions to eliminate enteric pathogens, strengthen epithelial barrier function, or block enteric pathogens-induced intestinal inflammation are encouraged.
Topic Editor Arun K. Bhunia receives financial support from BioMatrix International and United Animal Health and holds patents. The other Topic Editor declares no competing interests with regard to the Research Topic subject.