Inflammation is one of the most fundamental and significant protective reactions of the organism to eradicate the source of damage and restore tissue function. The persistence of inflammation can lead to tissue and organ damage. Therefore, inflammation is often associated with the development and progression of a series of functional gastrointestinal disorders or digestive tract diseases, such as irritable bowel syndrome, inflammatory bowel disease, necrotizing enterocolitis, gastro-esophageal reflux, Helicobacter pylori infection, etc. Pathogenesis ensues when there is prolonged or excessive inflammation in the gut. Gastrointestinal inflammation can be caused by many factors, including chemical, mechanical or microbial damage, neurological, endocrine, or immune disorder, and especially many pathogen infections like viruses, bacteria, fungi, and protozoa. Inflammation in the gastrointestinal tract can induce tissue damage and dysfunction. Chronic bowel inflammation even causes irreversible fibrosis, such as Crohn's disease, inflammatory bowel disease, etc.
A great number of microbial species live in the gastrointestinal tract. Dysbiosis of the gut microbiota strongly affects our health and disease status. The gastrointestinal tract is susceptible to bacterial infection. Although gut bacteria often drive immune activation, chronic inflammation in turn shapes the gut microbiota and contributes to dysbiosis. However, the host-microbial relationships relevant to human gastrointestinal functional disease are far from clear. A better understanding of the role of inflammation and its components in these related gastrointestinal diseases might provide a more complete picture of the mechanisms of these disorders and lay the foundation for novel therapies.
This Research Topic welcomes submissions of research papers describing new findings on pathophysiological pathways, processes, and solutions to inflammation-based gut functional disorders, including but not limited to the following:
• Effects of inflammation (e.g., immune cells, cytokines, related receptors, molecules, hormones, genes, nuclei) on gastrointestinal mucosa barrier, secretion, and motor functions;
• Causes and processes of inflammation-related gastrointestinal dysfunctions (e.g., gut dysbiosis, Helicobacter pylori-infection, etc.);
• Immune, neurological, and endocrine-related mechanisms affecting gastrointestinal function under inflammation;
• Host-microbial relationships relevant to human gastrointestinal function disease;
• Novel approaches to the treatment of inflammation-related gastrointestinal functional disorders (e.g., Crohn's disease, ulcerative colitis, necrotizing enterocolitis, gastro-esophageal reflux, Helicobacter pylori-infected functional dyspepsia ).
Inflammation is one of the most fundamental and significant protective reactions of the organism to eradicate the source of damage and restore tissue function. The persistence of inflammation can lead to tissue and organ damage. Therefore, inflammation is often associated with the development and progression of a series of functional gastrointestinal disorders or digestive tract diseases, such as irritable bowel syndrome, inflammatory bowel disease, necrotizing enterocolitis, gastro-esophageal reflux, Helicobacter pylori infection, etc. Pathogenesis ensues when there is prolonged or excessive inflammation in the gut. Gastrointestinal inflammation can be caused by many factors, including chemical, mechanical or microbial damage, neurological, endocrine, or immune disorder, and especially many pathogen infections like viruses, bacteria, fungi, and protozoa. Inflammation in the gastrointestinal tract can induce tissue damage and dysfunction. Chronic bowel inflammation even causes irreversible fibrosis, such as Crohn's disease, inflammatory bowel disease, etc.
A great number of microbial species live in the gastrointestinal tract. Dysbiosis of the gut microbiota strongly affects our health and disease status. The gastrointestinal tract is susceptible to bacterial infection. Although gut bacteria often drive immune activation, chronic inflammation in turn shapes the gut microbiota and contributes to dysbiosis. However, the host-microbial relationships relevant to human gastrointestinal functional disease are far from clear. A better understanding of the role of inflammation and its components in these related gastrointestinal diseases might provide a more complete picture of the mechanisms of these disorders and lay the foundation for novel therapies.
This Research Topic welcomes submissions of research papers describing new findings on pathophysiological pathways, processes, and solutions to inflammation-based gut functional disorders, including but not limited to the following:
• Effects of inflammation (e.g., immune cells, cytokines, related receptors, molecules, hormones, genes, nuclei) on gastrointestinal mucosa barrier, secretion, and motor functions;
• Causes and processes of inflammation-related gastrointestinal dysfunctions (e.g., gut dysbiosis, Helicobacter pylori-infection, etc.);
• Immune, neurological, and endocrine-related mechanisms affecting gastrointestinal function under inflammation;
• Host-microbial relationships relevant to human gastrointestinal function disease;
• Novel approaches to the treatment of inflammation-related gastrointestinal functional disorders (e.g., Crohn's disease, ulcerative colitis, necrotizing enterocolitis, gastro-esophageal reflux, Helicobacter pylori-infected functional dyspepsia ).
