The mucosal epithelial barrier is the first line of defense against pathogens, xenobiotic, and dietary components. The alimentary tract contains the barrier-based defense system, closely associated with the mucosal immune systems composed of immune cells, complement, and cytokines, playing important roles in regulating human pathophysiology. Discordant regulation of this network or epithelial inflammatory dysregulation would lead to various types of mucosa-associated or systemic diseases. The recent scientific advances have greatly increased our understanding of epithelial inflammatory responses. In particular, the ecology of microbiota is one of the pivotal modulator of epithelial inflammation and physiology in human health and diseases. Various types of pattern recognition receptor (PRR)-linked or stress-responsive signaling pathways have been shown to be involved in epithelial homeostasis or pathogenesis during human gut disorders. Accordingly, recognition of pathogen-associated molecular patterns (PAMPs) from microbiota via PRR can modulate inflammatory responses against bacteria and intestinal homeostasis through signaling pathways, activating NF?B, AP1 and IRF3 transcription factors. Moreover, diet or microbe-derived metabolites, such as short-chain fatty acids (SCFAs), can be recognized by G-protein coupled receptors (GPCRs) or transported into epithelial cells, respectively, inducing cell proliferation, epithelial barrier function, and energy source, among others. Additionally, enteroendocrine cells (EECs) are the most abundant form of endocrine cells as a subset of the enteric nervous system although they only make up 1% of that epithelium. EECs as the chemoreceptor secrete gastrointestinal hormones and peptides which regulate gastrointestinal nervous, metabolic, and immune response to the luminal contents including nutrients, xenobiotic agents, and microbiota. The above examples are a sample of the diverse range of communication that intestinal epithelial cells have with their environment, including signals from the lumen, other cells or the microbiota.
We welcome authors to submit Original Research, Review and Method articles that seek to define the novel molecular pathways of epithelial inflammation and mucosal networks in the healthy and diseased gut niche during infection, dysbiosis, hypersensitivity, immune suppression, degenerative diseases, cancers, and other acute or chronic diseases. We particularly welcome studies covering Molecular Pathways in:
1. Gut epithelial immunity and barrier to diet, xenobiotic, and microbiota
2. Gut epithelial inflammation by microbes and endogenous triggers
3. Gut mucosal immune crosstalk with other regulatory networks such as neuroendocrine systems in health and disease
4. Gut epithelial inflammation and immunity in cancer, metabolic diseases, and autoimmune diseases.
The mucosal epithelial barrier is the first line of defense against pathogens, xenobiotic, and dietary components. The alimentary tract contains the barrier-based defense system, closely associated with the mucosal immune systems composed of immune cells, complement, and cytokines, playing important roles in regulating human pathophysiology. Discordant regulation of this network or epithelial inflammatory dysregulation would lead to various types of mucosa-associated or systemic diseases. The recent scientific advances have greatly increased our understanding of epithelial inflammatory responses. In particular, the ecology of microbiota is one of the pivotal modulator of epithelial inflammation and physiology in human health and diseases. Various types of pattern recognition receptor (PRR)-linked or stress-responsive signaling pathways have been shown to be involved in epithelial homeostasis or pathogenesis during human gut disorders. Accordingly, recognition of pathogen-associated molecular patterns (PAMPs) from microbiota via PRR can modulate inflammatory responses against bacteria and intestinal homeostasis through signaling pathways, activating NF?B, AP1 and IRF3 transcription factors. Moreover, diet or microbe-derived metabolites, such as short-chain fatty acids (SCFAs), can be recognized by G-protein coupled receptors (GPCRs) or transported into epithelial cells, respectively, inducing cell proliferation, epithelial barrier function, and energy source, among others. Additionally, enteroendocrine cells (EECs) are the most abundant form of endocrine cells as a subset of the enteric nervous system although they only make up 1% of that epithelium. EECs as the chemoreceptor secrete gastrointestinal hormones and peptides which regulate gastrointestinal nervous, metabolic, and immune response to the luminal contents including nutrients, xenobiotic agents, and microbiota. The above examples are a sample of the diverse range of communication that intestinal epithelial cells have with their environment, including signals from the lumen, other cells or the microbiota.
We welcome authors to submit Original Research, Review and Method articles that seek to define the novel molecular pathways of epithelial inflammation and mucosal networks in the healthy and diseased gut niche during infection, dysbiosis, hypersensitivity, immune suppression, degenerative diseases, cancers, and other acute or chronic diseases. We particularly welcome studies covering Molecular Pathways in:
1. Gut epithelial immunity and barrier to diet, xenobiotic, and microbiota
2. Gut epithelial inflammation by microbes and endogenous triggers
3. Gut mucosal immune crosstalk with other regulatory networks such as neuroendocrine systems in health and disease
4. Gut epithelial inflammation and immunity in cancer, metabolic diseases, and autoimmune diseases.
