FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2563721064> ?p ?o ?g. }

• W2563721064 abstract "Bile acids, important mediators of lipid absorption, also act as hormone-like regulators and as antimicrobial molecules. In all these functions their potency is modulated by a variety of chemical modifications catalyzed by bacteria of the healthy gut microbiota, generating a complex variety of secondary bile acids. Intestinal commensal organisms are well adapted to normal concentrations of bile acids in the gut. In contrast, physiological concentrations of the various intestinal bile acid species play an important role in the resistance to intestinal colonization by pathogens such as Clostridium difficile. Antibiotic therapy can perturb the gut microbiota and thereby impair the production of protective secondary bile acids. The most important bile acid transformation is 7-dehydroxylation, producing deoxycholic acid and lithocholic acid. The enzymatic pathway carrying out 7-dehydroxylation is restricted to a narrow phylogenetic group of commensal bacteria, the best-characterized of which is Clostridium scindens. Like many other intestinal commensal species, 7-dehydroxylating bacteria are understudied in vivo. Conventional animals contain variable and uncharacterized indigenous 7-dehydroxylating organisms that cannot be selectively removed, making controlled colonization with a specific strain in the context of an undisturbed microbiota unfeasible. In the present study, we used a recently established, standardized gnotobiotic mouse model that is stably associated with a simplified murine 12-species oligo-mouse microbiota (Oligo-MM12). It is representative of the major murine intestinal bacterial phyla, but is deficient for 7-dehydroxylation. We find that the Oligo-MM12 consortium carries out bile acid deconjugation, a prerequisite for 7-dehydroxylation, and confers no resistance to C. difficile infection (CDI). Amendment of Oligo-MM12 with C. scindens normalized the large intestinal bile acid composition by reconstituting 7-dehydroxylation. These changes had only minor effects on the composition of the native Oligo-MM12, but significantly decreased early large intestinal C. difficile colonization and pathogenesis. The delayed pathogenesis of C. difficile in C. scindens-colonized mice was associated with breakdown of cecal microbial bile acid transformation." @default.
• W2563721064 created "2017-01-06" @default.
• W2563721064 creator A5007365355 @default.
• W2563721064 creator A5018058165 @default.
• W2563721064 creator A5019246564 @default.
• W2563721064 creator A5019984620 @default.
• W2563721064 creator A5036827804 @default.
• W2563721064 creator A5039213727 @default.
• W2563721064 creator A5039795688 @default.
• W2563721064 creator A5044949409 @default.
• W2563721064 creator A5053083037 @default.
• W2563721064 creator A5065088339 @default.
• W2563721064 creator A5073430364 @default.
• W2563721064 creator A5079237100 @default.
• W2563721064 creator A5080389668 @default.
• W2563721064 date "2016-12-20" @default.
• W2563721064 modified "2023-10-14" @default.
• W2563721064 title "Functional Intestinal Bile Acid 7α-Dehydroxylation by Clostridium scindens Associated with Protection from Clostridium difficile Infection in a Gnotobiotic Mouse Model" @default.
• W2563721064 cites W1510622110 @default.
• W2563721064 cites W1529695053 @default.
• W2563721064 cites W1705744822 @default.
• W2563721064 cites W1880946804 @default.
• W2563721064 cites W1968953113 @default.
• W2563721064 cites W1969668125 @default.
• W2563721064 cites W1974402925 @default.
• W2563721064 cites W1979012796 @default.
• W2563721064 cites W1982203245 @default.
• W2563721064 cites W1984345984 @default.
• W2563721064 cites W1986150323 @default.
• W2563721064 cites W1987904060 @default.
• W2563721064 cites W1993830991 @default.
• W2563721064 cites W1993980462 @default.
• W2563721064 cites W2000335726 @default.
• W2563721064 cites W2026894676 @default.
• W2563721064 cites W2034730227 @default.
• W2563721064 cites W2071273298 @default.
• W2563721064 cites W2085178117 @default.
• W2563721064 cites W2087577664 @default.
• W2563721064 cites W2088454480 @default.
• W2563721064 cites W2097297514 @default.
• W2563721064 cites W2102818798 @default.
• W2563721064 cites W2106515170 @default.
• W2563721064 cites W2122138398 @default.
• W2563721064 cites W2122674349 @default.
• W2563721064 cites W2124519481 @default.
• W2563721064 cites W2124954246 @default.
• W2563721064 cites W2139566520 @default.
• W2563721064 cites W2149529467 @default.
• W2563721064 cites W2149711482 @default.
• W2563721064 cites W2154304430 @default.
• W2563721064 cites W2162904770 @default.
• W2563721064 cites W2166520113 @default.
• W2563721064 cites W2168420558 @default.
• W2563721064 cites W2170276816 @default.
• W2563721064 cites W2171605634 @default.
• W2563721064 cites W2174287538 @default.
• W2563721064 cites W2253934566 @default.
• W2563721064 cites W2268645719 @default.
• W2563721064 cites W2292760617 @default.
• W2563721064 cites W2310948435 @default.
• W2563721064 cites W2336367423 @default.
• W2563721064 cites W2526966274 @default.
• W2563721064 cites W2549269050 @default.
• W2563721064 cites W958079127 @default.
• W2563721064 doi "https://doi.org/10.3389/fcimb.2016.00191" @default.
• W2563721064 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5168579" @default.
• W2563721064 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28066726" @default.
• W2563721064 hasPublicationYear "2016" @default.
• W2563721064 type Work @default.
• W2563721064 sameAs 2563721064 @default.
• W2563721064 citedByCount "127" @default.
• W2563721064 countsByYear W25637210642017 @default.
• W2563721064 countsByYear W25637210642018 @default.
• W2563721064 countsByYear W25637210642019 @default.
• W2563721064 countsByYear W25637210642020 @default.
• W2563721064 countsByYear W25637210642021 @default.
• W2563721064 countsByYear W25637210642022 @default.
• W2563721064 countsByYear W25637210642023 @default.
• W2563721064 crossrefType "journal-article" @default.
• W2563721064 hasAuthorship W2563721064A5007365355 @default.
• W2563721064 hasAuthorship W2563721064A5018058165 @default.
• W2563721064 hasAuthorship W2563721064A5019246564 @default.
• W2563721064 hasAuthorship W2563721064A5019984620 @default.
• W2563721064 hasAuthorship W2563721064A5036827804 @default.
• W2563721064 hasAuthorship W2563721064A5039213727 @default.
• W2563721064 hasAuthorship W2563721064A5039795688 @default.
• W2563721064 hasAuthorship W2563721064A5044949409 @default.
• W2563721064 hasAuthorship W2563721064A5053083037 @default.
• W2563721064 hasAuthorship W2563721064A5065088339 @default.
• W2563721064 hasAuthorship W2563721064A5073430364 @default.
• W2563721064 hasAuthorship W2563721064A5079237100 @default.
• W2563721064 hasAuthorship W2563721064A5080389668 @default.
• W2563721064 hasBestOaLocation W25637210641 @default.
• W2563721064 hasConcept C151730666 @default.
• W2563721064 hasConcept C189506811 @default.
• W2563721064 hasConcept C2777165150 @default.
• W2563721064 hasConcept C2779343474 @default.
• W2563721064 hasConcept C2779399885 @default.
• W2563721064 hasConcept C2780420665 @default.
• W2563721064 hasConcept C2780749602 @default.

• next