Summary of Study ST002345

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001505. The data can be accessed directly via it's Project DOI: 10.21228/M85717 This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002345
Study TitleStress-Induced Mucosal Layer Disruption Drives Gut Dysbiosis and Depressive-like Behaviors
Study SummaryDepression is a common mental health condition with a large social and economic impact. While depression etiology is multifactorial, chronic stress is a well-accepted contributor to disease onset. In addition, depression is associated with altered gut microbial signatures that can be replicated in animal models. While targeted restoration of the microbiome has been shown to reduce depressive-like behaviors in mice, the complexity and diversity of the human microbiome has complicated therapeutic intervention in patients. To circumvent these limitations, there is a critical need for identifying pathways responsible for microbiome dysbiosis. Here, for the first time, we identify the changes in host physiology that induce microbiome dysbiosis. Specifically, we show that a component of mucosal layer, the transmembrane protein mucin 13, can regulate microbiome composition. Using a model of chronic stress to induce behavioral and microbial changes in mice, we show a significant reduction in mucin 13 expression across the intestines that occurs independently of the microbiome. Furthermore, deleting Muc13 leads to gut dysbiosis, and baseline behavioral changes normally observed after stress exposure. Together, these results validate the hypothesis that mucosal layer disruption is an initiating event in stress-induced dysbiosis and offer mucin 13 as a potential new therapeutic target for microbiome dysbiosis in stress-induced depression. For the first time, our data provide an upstream and conserved target for treating microbiome dysbiosis, a result with sweeping implications for diseases presenting with microbial alterations.
University of Virginia
Last NameRivet-Noor
First NameCourtney
Address409 Lane Road, Charlottsville, Virginia, 22903, USA
Submit Date2022-11-10
Num Groups2
Total Subjects23
Num Males23
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2022-11-28
Release Version1
Courtney Rivet-Noor Courtney Rivet-Noor application/zip

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Combined analysis:

Analysis ID AN003829
Analysis type MS
Chromatography type Reversed phase
Chromatography system Thermo Vanquish
Column Waters Acquity BEH C18 (100 x 2mm,1.7um)
MS instrument type Orbitrap
MS instrument name Thermo Orbitrap ID-X tribrid
Units ug/mL


Chromatography ID:CH002834
Instrument Name:Thermo Vanquish
Column Name:Waters Acquity BEH C18 (100 x 2mm,1.7um)
Flow Gradient:0min: 0% B, 8min: 50% B, 9 min: 98% B, 13min: 98% B. Recalibration of system up to 15 min at 0% B for next injection.
Solvent A:100% water; 0.1% formic acid
Solvent B:100% methanol 0.1% formic acid
Analytical Time:15 min
Chromatography Type:Reversed phase