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Journal ArticleDOI

Differences in goblet cell differentiation between Crohn's disease and ulcerative colitis.

TLDR
Both transcription factors are key regulators of goblet cell differentiation and mucin formation in the human colon, and inflammation is associated with an enhanced gobleT cell differentiation in CD but not in UC, a defect possibly of pathogenic importance.
About
This article is published in Differentiation.The article was published on 2009-01-01. It has received 240 citations till now. The article focuses on the topics: Goblet cell & Mucin.

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Citations
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Journal ArticleDOI

Homeostasis and Inflammation in the Intestine

TL;DR: This Review considers the many cellular and molecular methods by which inflammatory responses are regulated to maintain intestinal homeostasis and the disease states that can ensue when this balance is lost.
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Epithelial IL-18 Equilibrium Controls Barrier Function in Colitis.

TL;DR: It is shown that IL-18 is critical in driving the pathologic breakdown of barrier integrity in a model of colitis, and the mechanism of goblet cell dysfunction that underlies the pathology of ulcerative colitis is informed on.
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Mechanisms and consequences of intestinal dysbiosis

TL;DR: The characterization of the changes leading to intestinal dysbiosis and the identification of the microbial taxa contributing to pathological effects are essential prerequisites to better understand the impact of the microbiota on health and disease.
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Intestinal barrier in inflammatory bowel disease.

TL;DR: This review provides an overview about the major components of this protective system as for example an intact epithelium, the synthesis of various antimicrobial peptides and the formation of the mucus layer and the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease.
References
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Journal ArticleDOI

A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease

TL;DR: It is shown that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease, and a link between an innate immune response to bacterial components and development of disease is suggested.
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Unravelling the pathogenesis of inflammatory bowel disease

TL;DR: Recently, substantial advances in the understanding of the molecular pathogenesis of inflammatory bowel disease (IBD) have been made owing to three related lines of investigation as mentioned in this paper, which have shown the importance of epithelial barrier function, and innate and adaptive immunity in disease pathogenesis.
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Mucosal flora in inflammatory bowel disease

TL;DR: It is hypothesized that the healthy mucosa is capable of holding back fecal bacteria and that this function is profoundly disturbed in patients with IBD, suggesting that the changes in the mucosal flora in IBD are not secondary to inflammation, but a result of a specific host response.
Journal ArticleDOI

The fundamental basis of inflammatory bowel disease

TL;DR: It is concluded that IBD is indeed characterized by an abnormal mucosal immune response but that microbial factors and epithelial cell abnormalities can facilitate this response.
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