Summary of Study ST003425
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002117. The data can be accessed directly via it's Project DOI: 10.21228/M8ZV6G This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
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.
Study ID | ST003425 |
Study Title | Targeted free fatty acids metabolomics studies on serum, cecal content, cecum tissue, chow diet, and Tritrichomonas mu cells |
Study Summary | Serum, cecal content, cecum tissue samples of murine, chow diet, and T.mu cells were collected to perform the targeted free fatty acids metabolome analysis. The aim of this study was to verify that whether T.mu could release free PUFA (especially ARA) to the intestinal tract of its host by comparing the PUFA concentration in the freshly isolated T.mu cells, chow diet, cecal content and serum of the host (Mus musculus).Based on the result of this targeted free fatty acids metabolomics studies, we found that T.mu could release ARA to the intestinal tract of its host and increase the concentration of ARA in its host's intestinal tract. |
Institute | Xuzhou medical university |
Last Name | Kou |
First Name | Yanbo |
Address | Tongshan road 209, Xuzhou, Jiangsu, 221004, China |
fightingkyb@163.com | |
Phone | +86-051683262123 |
Submit Date | 2024-08-20 |
Raw Data Available | Yes |
Raw Data File Type(s) | cdf |
Analysis Type Detail | GC-MS |
Release Date | 2024-09-10 |
Release Version | 1 |
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Project:
Project ID: | PR002117 |
Project DOI: | doi: 10.21228/M8ZV6G |
Project Title: | A mouse protozoan boosts antigen-specific mucosal IgA responses in a specific lipid metabolism- and signaling-dependent manner |
Project Summary: | IgA antibodies play an important role in mucosal immunity. However, there is still no effective way to consistently boost mucosal IgA responses, and the factors influencing these responses are not fully understood. We observed that colonization with the murine intestinal symbiotic protozoan Tritrichomonas musculis (T.mu) boosted antigen-specific mucosal IgA responses in wild-type C57BL/6 mice. This enhancement was attributed to the accumulation of free arachidonic acid (ARA) in the intestinal lumen, which served as a signal to stimulate the production of antigen-specific mucosal IgA. When ARA was prevented from undergoing its downstream metabolic transformation using the 5-lipoxygenase inhibitor zileuton or by blocking its downstream biological signaling through genetic deletion of the Leukotriene B4 receptor 1 (Blt1), the T.mu-mediated enhancement of antigen-specific mucosal IgA production was suppressed. Moreover, both T.mu transfer and dietary supplementation of ARA augmented the efficacy of an oral vaccine against Salmonella infection, with this effect being dependent on Blt1. Our findings elucidate a tripartite circuit linking nutrients from the diet or intestinal microbiota, host lipid metabolism, and the mucosal humoral immune response. |
Institute: | Xuzhou medical university |
Last Name: | Kou |
First Name: | Yanbo |
Address: | Tongshan road 209, Xuzhou, Jiangsu, 221004, China |
Email: | fightingkyb@163.com |
Phone: | +86-051683262123 |