The gastrointestinal (GI) mucosa is a protective semipermeable barrier that allows interactions between humans and the external world and protects against invading microorganisms and their toxins as well as virus and their pathogenic epitopes. It is composed of various layers with specific roles, providing sustenance, defense, and health. The dynamic interplay between structural components of the GI mucosa and molecular mechanisms ensures integrity and immunological homeostasis.
However, GI barrier function may be damaged by subtle or severe alterations, including structural lesions, chemical substances, parasite invasion, or alteration of the gut microbiota composition and function, resulting in changes that may compromise the mucosal protective regulatory components and alterations of the GI homeostatic balance. These alterations have been associated with a wide variety of diseases, including GI diseases (e.g. oral diseases, gastroesophageal reflux disease, ulcerative colitis, Crohn's disease, mucositis, infectious and noninfectious diarrhea, allergic diseases, etc) and non-GI diseases (e.g. obesity, type 1 diabetes, chronic liver disease, etc); and interestingly, all these diseases are associated with inflammation that might have been triggered by the invasion of luminal microbial components and exaggerated activation of the GI immune response.
This Research Topic will contribute to an increase understanding of how alterations in the GI barrier can contribute to the development of intestinal and non-intestinal inflammatory diseases. We welcome original articles, mini-reviews, reviews, commentaries, and perspectives in the preclinical, translational, and clinical field that explore, but are not limited to, how defects in the GI barrier can contribute to the development of intestinal and non-intestinal inflammatory diseases.
The gastrointestinal (GI) mucosa is a protective semipermeable barrier that allows interactions between humans and the external world and protects against invading microorganisms and their toxins as well as virus and their pathogenic epitopes. It is composed of various layers with specific roles, providing sustenance, defense, and health. The dynamic interplay between structural components of the GI mucosa and molecular mechanisms ensures integrity and immunological homeostasis.
However, GI barrier function may be damaged by subtle or severe alterations, including structural lesions, chemical substances, parasite invasion, or alteration of the gut microbiota composition and function, resulting in changes that may compromise the mucosal protective regulatory components and alterations of the GI homeostatic balance. These alterations have been associated with a wide variety of diseases, including GI diseases (e.g. oral diseases, gastroesophageal reflux disease, ulcerative colitis, Crohn's disease, mucositis, infectious and noninfectious diarrhea, allergic diseases, etc) and non-GI diseases (e.g. obesity, type 1 diabetes, chronic liver disease, etc); and interestingly, all these diseases are associated with inflammation that might have been triggered by the invasion of luminal microbial components and exaggerated activation of the GI immune response.
This Research Topic will contribute to an increase understanding of how alterations in the GI barrier can contribute to the development of intestinal and non-intestinal inflammatory diseases. We welcome original articles, mini-reviews, reviews, commentaries, and perspectives in the preclinical, translational, and clinical field that explore, but are not limited to, how defects in the GI barrier can contribute to the development of intestinal and non-intestinal inflammatory diseases.