scispace - formally typeset
Open AccessJournal ArticleDOI

The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria

Reads0
Chats0
TLDR
Findings show that the Muc2 mucin can build a mucus barrier that separates bacteria from the colon epithelia and suggest that defects in this mucus can cause colon inflammation.
Abstract
We normally live in symbiosis with approximately 10(13) bacteria present in the colon. Among the several mechanisms maintaining the bacteria/host balance, there is limited understanding of the structure, function, and properties of intestinal mucus. We now demonstrate that the mouse colonic mucus consists of two layers extending 150 mum above the epithelial cells. Proteomics revealed that both of these layers have similar protein composition, with the large gel-forming mucin Muc2 as the major structural component. The inner layer is densely packed, firmly attached to the epithelium, and devoid of bacteria. In contrast, the outer layer is movable, has an expanded volume due to proteolytic cleavages of the Muc2 mucin, and is colonized by bacteria. Muc2(-/-) mice have bacteria in direct contact with the epithelial cells and far down in the crypts, explaining the inflammation and cancer development observed in these animals. These findings show that the Muc2 mucin can build a mucus barrier that separates bacteria from the colon epithelia and suggest that defects in this mucus can cause colon inflammation.

read more

Citations
More filters
Journal ArticleDOI

Interactions between the microbiota and the immune system.

TL;DR: Advances in understanding of the interactions between resident microbes and the immune system are reviewed and the implications for human health are reviewed.
Journal ArticleDOI

Gut Microbiota in Health and Disease

TL;DR: The advances in modeling and analysis of gut microbiota will further the authors' knowledge of their role in health and disease, allowing customization of existing and future therapeutic and prophylactic modalities.
Journal ArticleDOI

Intestinal mucosal barrier function in health and disease.

TL;DR: Recent advances have uncovered mechanisms by which the intestinal mucosal barrier is regulated in response to physiological and immunological stimuli, along with evidence that this regulation shapes mucosal immune responses in the gut and, when dysfunctional, may contribute to disease.
Journal ArticleDOI

The gut microbiota — masters of host development and physiology

TL;DR: The gut microbiota has a beneficial role during normal homeostasis, modulating the host's immune system as well as influencing host development and physiology, including organ development and morphogenesis, and host metabolism.
Journal ArticleDOI

Intestinal epithelial cells: regulators of barrier function and immune homeostasis

TL;DR: This Review provides a comprehensive overview of how IECs maintain host–commensal microbial relationships and immune cell homeostasis in the intestine.
References
More filters
Journal ArticleDOI

Host-Bacterial Mutualism in the Human Intestine

TL;DR: New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements the authors' biology in ways that are mutually beneficial.
Journal ArticleDOI

Combination of 16S rRNA-targeted oligonucleotide probes with flow cytometry for analyzing mixed microbial populations.

TL;DR: Fluorescent oligonucleotide hybridization probes were used to label bacterial cells for analysis by flow cytometry and the intensity of fluorescence was increased additively by the combined use of two or three fluorescent probes complementary to different regions of the same 16S rRNA.
Journal ArticleDOI

Inflammatory bowel disease: cause and immunobiology

TL;DR: How environmental factors, infectious microbes, ethnic origin, genetic susceptibility, and a dysregulated immune system can result in mucosal inflammation are discussed.
Journal ArticleDOI

Biochemistry and Genetics of von Willebrand Factor

TL;DR: Growing body of information about VWF synthesis, structure, and function has allowed the reclassification of VWD based upon distinct pathophysiologic mechanisms that appear to correlate with clinical symptoms and the response to therapy.
Related Papers (5)