Bifidobacteria exhibited stronger ability to utilize fructooligosaccharides, compared with other bacteria in the mouse intestine

2021 ◽  
Author(s):  
Jiayu Gu ◽  
Bingyong Mao ◽  
Shumao Cui ◽  
Xin Tang ◽  
Zhenmin Liu ◽  
...  
Keyword(s):  
Mouse Intestine

Commensal Flora Reduce E. coli O157:H7 and Shiga Toxin in Mouse Intestine

2006 ◽  
Vol 1 (4) ◽  
pp. 193-193
Keyword(s):  
Shiga Toxin ◽  
E Coli ◽  
Commensal Flora ◽  
Mouse Intestine

scholarly journals MetR-Regulated Vibrio cholerae Metabolism Is Required for Virulence

mBio ◽  
2012 ◽  
Vol 3 (5) ◽  
Author(s):  
Ryan W. Bogard ◽  
Bryan W. Davies ◽  
John J. Mekalanos
Keyword(s):  
Amino Acid ◽  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Current Knowledge ◽  
Intestinal Colonization ◽  
Wild Type ◽  
Pathogenic Potential ◽  
Content Type ◽  
Mouse Intestine

ABSTRACTLysR-type transcriptional regulators (LTTRs) are the largest, most diverse family of prokaryotic transcription factors, with regulatory roles spanning metabolism, cell growth and division, and pathogenesis. Using a sequence-defined transposon mutant library, we screened a panel ofV. choleraeEl Tor mutants to identify LTTRs required for host intestinal colonization. Surprisingly, out of 38 LTTRs, only one severely affected intestinal colonization in the suckling mouse model of cholera: the methionine metabolism regulator, MetR. Genetic analysis of genes influenced by MetR revealed thatglyA1andmetJwere also required for intestinal colonization. Chromatin immunoprecipitation of MetR and quantitative reverse transcription-PCR (qRT-PCR) confirmed interaction with and regulation ofglyA1, indicating that misregulation ofglyA1is likely responsible for the colonization defect observed in themetRmutant. TheglyA1mutant was auxotrophic for glycine but exhibited wild-type trimethoprim sensitivity, making folate deficiency an unlikely cause of its colonization defect. MetJ regulatory mutants are not auxotrophic but are likely altered in the regulation of amino acid-biosynthetic pathways, including those for methionine, glycine, and serine, and this misregulation likely explains its colonization defect. However, mutants defective in methionine, serine, and cysteine biosynthesis exhibited wild-type virulence, suggesting that these amino acids can be scavenged in vivo. Taken together, our results suggest that glycine biosynthesis may be required to alleviate an in vivo nutritional restriction in the mouse intestine; however, additional roles for glycine may exist. Irrespective of the precise nature of this requirement, this study illustrates the importance of pathogen metabolism, and the regulation thereof, as a virulence factor.IMPORTANCEVibrio choleraecontinues to be a severe cause of morbidity and mortality in developing countries. Identification ofV. choleraefactors critical to disease progression offers the potential to develop or improve upon therapeutics and prevention strategies. To increase the efficiency of virulence factor discovery, we employed a regulator-centric approach to multiplex our in vivo screening capabilities and allow whole regulons inV. choleraeto be interrogated for pathogenic potential. We identified MetR as a new virulence regulator and serine hydroxymethyltransferase GlyA1 as a new MetR-regulated virulence factor, both required byV. choleraeto colonize the infant mouse intestine. Bacterial metabolism is a prerequisite to virulence, and current knowledge of in vivo metabolism of pathogens is limited. Here, we expand the known role of amino acid metabolism and regulation in virulence and offer new insights into the in vivo metabolic requirements ofV. choleraewithin the mouse intestine.

scholarly journals Upregulation of Vitamin C Transporter Functional Expression in 5xFAD Mouse Intestine

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 617
Author(s):  
Trevor Teafatiller ◽  
Christopher W. Heskett ◽  
Anshu Agrawal ◽  
Jonathan S. Marchant ◽  
Janet E. Baulch ◽  
...  
Keyword(s):  
Mouse Model ◽  
Functional Expression ◽  
Specific Protein ◽  
Glutathione Peroxidase 1 ◽  
Stress Response Genes ◽  
Nuclear Rna ◽  
The Status ◽  
5Xfad Mouse ◽  
Mouse Intestine ◽  
5Xfad Mice

The process of obtaining ascorbic acid (AA) via intestinal absorption and blood circulation is carrier-mediated utilizing the AA transporters SVCT1 and SVCT2, which are expressed in the intestine and brain (SVCT2 in abundance). AA concentration is decreased in Alzheimer’s disease (AD), but information regarding the status of intestinal AA uptake in the AD is still lacking. We aimed here to understand how AA homeostasis is modulated in a transgenic mouse model (5xFAD) of AD. AA levels in serum from 5xFAD mice were markedly lower than controls. Expression of oxidative stress response genes (glutathione peroxidase 1 (GPX1) and superoxide dismutase 1 (SOD1)) were significantly increased in AD mice jejunum, and this increase was mitigated by AA supplementation. Uptake of AA in the jejunum was upregulated. This increased AA transport was caused by a marked increase in SVCT1 and SVCT2 protein, mRNA, and heterogeneous nuclear RNA (hnRNA) expression. A significant increase in the expression of HNF1α and specific protein 1 (Sp1), which drive SLC23A1 and SLC23A2 promoter activity, respectively, was observed. Expression of hSVCT interacting proteins GRHPR and CLSTN3 were also increased. SVCT2 protein and mRNA expression in the hippocampus of 5xFAD mice was not altered. Together, these investigations reveal adaptive up-regulation of intestinal AA uptake in the 5xFAD mouse model.

Lack of correlation between villus and crypt damage in irradiated mouse intestine

1979 ◽  
Vol 52 (618) ◽  
pp. 485-493 ◽  
Author(s):  
K. E. Carr ◽  
R. Hamlet ◽  
A. H. W. Nias ◽  
C. Watt
Keyword(s):  
Mouse Intestine

scholarly journals Effects of Tritrichomonas muris on the Mouse Intestine: A Proteomic Analysis

2009 ◽  
Vol 58 (5) ◽  
pp. 537-542 ◽  
Author(s):  
Akiko KASHIWAGI ◽  
Hajime KUROSAKI ◽  
Hong LUO ◽  
Hiroshi YAMAMOTO ◽  
Mitsuo OSHIMURA ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Mouse Intestine

scholarly journals Conversion of Daidzein and Genistein by an Anaerobic Bacterium Newly Isolated from the Mouse Intestine

2008 ◽  
Vol 74 (15) ◽  
pp. 4847-4852 ◽  
Author(s):  
Anastasia Matthies ◽  
Thomas Clavel ◽  
Michael Gütschow ◽  
Wolfram Engst ◽  
Dirk Haller ◽  
...  
Keyword(s):  
Stationary Phase ◽  
Enzyme Induction ◽  
Growth Phase ◽  
Anaerobic Bacterium ◽  
Stationary Growth Phase ◽  
Gut Bacteria ◽  
Soy Isoflavones ◽  
Strictly Anaerobic ◽  
Stationary Growth ◽  
Mouse Intestine

ABSTRACT The metabolism of isoflavones by gut bacteria plays a key role in the availability and bioactivation of these compounds in the intestine. Daidzein and genistein are the most common dietary soy isoflavones. While daidzein conversion yielding equol has been known for some time, the corresponding formation of 5-hydroxy-equol from genistein has not been reported previously. We isolated a strictly anaerobic bacterium (Mt1B8) from the mouse intestine which converted daidzein via dihydrodaidzein to equol as well as genistein via dihydrogenistein to 5-hydroxy-equol. Strain Mt1B8 was a gram-positive, rod-shaped bacterium identified as a member of the Coriobacteriaceae. Strain Mt1B8 also transformed dihydrodaidzein and dihydrogenistein to equol and 5-hydroxy-equol, respectively. The conversion of daidzein, genistein, dihydrodaidzein, and dihydrogenistein in the stationary growth phase depended on preincubation with the corresponding isoflavonoid, indicating enzyme induction. Moreover, dihydrogenistein was transformed even more rapidly in the stationary phase when strain Mt1B8 was grown on either genistein or daidzein. Growing the cells on daidzein also enabled conversion of genistein. This suggests that the same enzymes are involved in the conversion of the two isoflavones.

Proteomic identification of radiation response markers in mouse intestine and brain

PROTEOMICS ◽  
2011 ◽  
Vol 11 (7) ◽  
pp. 1254-1263 ◽  
Author(s):  
Young-Bin Lim ◽  
Bo-Jeong Pyun ◽  
Hae-June Lee ◽  
Sang-Rok Jeon ◽  
Yeung Bae Jin ◽  
...  
Keyword(s):  
Radiation Response ◽  
Mouse Intestine ◽  
Proteomic Identification

scholarly journals Glycolipid-dependent and lectin-driven transcytosis in mouse enterocytes

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Alena Ivashenka ◽  
Christian Wunder ◽  
Valerie Chambon ◽  
Roger Sandhoff ◽  
Richard Jennemann ◽  
...  
Keyword(s):  
Basolateral Membrane ◽  
Intestinal Barrier ◽  
Growth Factor Signaling ◽  
Dependent Manner ◽  
Galectin 3 ◽  
Cell Adhesion And Migration ◽  
Range Of Functions ◽  
Mouse Intestine ◽  
And Migration

AbstractGlycoproteins and glycolipids at the plasma membrane contribute to a range of functions from growth factor signaling to cell adhesion and migration. Glycoconjugates undergo endocytic trafficking. According to the glycolipid-lectin (GL-Lect) hypothesis, the construction of tubular endocytic pits is driven in a glycosphingolipid-dependent manner by sugar-binding proteins of the galectin family. Here, we provide evidence for a function of the GL-Lect mechanism in transcytosis across enterocytes in the mouse intestine. We show that galectin-3 (Gal3) and its newly identified binding partner lactotransferrin are transported in a glycosphingolipid-dependent manner from the apical to the basolateral membrane. Transcytosis of lactotransferrin is perturbed in Gal3 knockout mice and can be rescued by exogenous Gal3. Inside enterocytes, Gal3 is localized to hallmark structures of the GL-Lect mechanism, termed clathrin-independent carriers. These data pioneer the existence of GL-Lect endocytosis in vivo and strongly suggest that polarized trafficking across the intestinal barrier relies on this mechanism.

The Effect of Vibrio Comma Mucinase upon the Permeability of Mouse Intestine

1955 ◽  
Vol 97 (3) ◽  
pp. 268-273 ◽  
Author(s):  
G. T. Lam ◽  
R. J. Mandle ◽  
K. Goodner
Keyword(s):  
Mouse Intestine
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