Dataset Information

Fiber-associated microbiota protects against diet-induced amelioration of the colonic mucus barrier

ABSTRACT: Here we have shown that diet-mediated alterations of the gut microbiota composition cause an erosion of the colonic mucus barrier. A compensatory increase in cellular mucus production by the host is not sufficient to re-establish the barrier, possibly due to a lacking increase in mucus secretion. While microbial transplant from mice fed a fiber-rich diet can prevent the mucus defects, the mechanism seems to be independent of general fiber fermentation and rather depend on distinct bacterial species and/or their metabolites.

OTHER RELATED OMICS DATASETS IN: PRJEB20367

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Colon, Colonic Mucosa

SUBMITTER: Liisa Arike

LAB HEAD: Liisa Arike

PROVIDER: PXD006129 | Pride | 2017-12-22

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	160324_QEx_LA_MS556_02.raw	Raw
	160324_QEx_LA_MS556_04.raw	Raw
	160324_QEx_LA_MS556_06.raw	Raw
	160324_QEx_LA_MS556_08.raw	Raw
	160324_QEx_LA_MS556_10.raw	Raw

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Publications

Bifidobacteria or Fiber Protects against Diet-Induced Microbiota-Mediated Colonic Mucus Deterioration.

Schroeder Bjoern O BO Birchenough George M H GMH Ståhlman Marcus M Arike Liisa L Johansson Malin E V MEV Hansson Gunnar C GC Bäckhed Fredrik F

Cell host & microbe 20171221 1

Diet strongly affects gut microbiota composition, and gut bacteria can influence the colonic mucus layer, a physical barrier that separates trillions of gut bacteria from the host. However, the interplay between a Western style diet (WSD), gut microbiota composition, and the intestinal mucus layer is less clear. Here we show that mice fed a WSD have an altered colonic microbiota composition that causes increased penetrability and a reduced growth rate of the inner mucus layer. Both barrier defec ...[more]

PMID: 29276171

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Project description:In this study we compared the intestinal mucus phenotype of Clca1-deficient (Clca1-/-) mice and wild-type (WT) controls. The human CLCA1 (chloride channel regulator, calcium-activated) and its murine ortholog mouse CLCA1 (formerly known as CLCA3) are secreted proteins which have been linked to human respiratory diseases such as asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) as well as to the corresponding murine models of these diseases. Common, disease severity-related features are goblet cell hyperplasia, mucus overproduction and disturbed clearance. Neutralization of mouse CLCA1 ameliorates the symptoms in the asthmatic mouse model and restoration of the decreased mouse CLCA1 protein level in a CF mouse model ameliorates the intestinal CF lesions, pointing toward these proteins being potential therapeutic targets. The expression CLCA1 can be induced in airways but this protein is normally expressed and secreted by goblet cells of the intestinal tract in both human and mouse together with the intestinal MUC2 mucin. This makes CLCA1 a major constituent of the extracellular intestinal mucus in which the MUC2 mucin is the main structural component. To study the possible further effects of murine CLCA1 deficiency on Muc2 and on other important components of the mucus, such as Agr2, Fcgbp, Klk and Zg16, a shotgun label-free proteomics study was performed which compared their relative abundance in the mucus layer, showing a tight and significant correlation between WT and Clca1-/- mucus proteins (Pearson r = 0.931, r2 = 0.868, p < 0.0001, based on 809 valid pairs). No significant differences in known mucus protein expression were observed. However, the abundance of CLCA1 in the mucus together with the domain structure suggests a structural role and other methods to reveal the function of these domains might shed light on the overall function in mucus. Because of its abundance in the mucus and the well preserved structure thought a long evolution together with mucus we still speculate that CLCA1 was developed to protect the expressing organism, although the threat is elusive.