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A Multihit Model: Colitis Lessons from the Interleukin-10–deficient Mouse

Complex mechanisms are pulling the strings to initiate the development of inflammatory bowel disease. Current evidence indicates that an interaction of genetic susceptibilities (polymorphisms), environmental factors, and the host microbiota leads to a dysregulation of the mucosal immune system. In t...

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Detalles Bibliográficos
Autores principales: Keubler, Lydia M., Buettner, Manuela, Häger, Christine, Bleich, André
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511684/
https://www.ncbi.nlm.nih.gov/pubmed/26164667
http://dx.doi.org/10.1097/MIB.0000000000000468
Descripción
Sumario:Complex mechanisms are pulling the strings to initiate the development of inflammatory bowel disease. Current evidence indicates that an interaction of genetic susceptibilities (polymorphisms), environmental factors, and the host microbiota leads to a dysregulation of the mucosal immune system. In the past decades, the interleukin-10–deficient mouse has served as an excellent model to mirror the multifactorial nature of this disease. Here, we want to review in detail the interplay of the genetic factors, immune aspects, and especially summarize and discuss the role of the microbiota contributing to colitis development in the interleukin-10–deficient mouse model of inflammatory bowel disease as a multihit model.