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020 ▼a 9781392713532
035 ▼a (MiAaPQ)AAI22583774
040 ▼a MiAaPQ ▼c MiAaPQ ▼d 247004
0820 ▼a 574
1001 ▼a Ehrlich, Amy Melissa.
24510 ▼a Microbial Metabolites Influence of Microbial Metabolites on the Gut-brain Axis.
260 ▼a [S.l.]: ▼b University of California, Davis., ▼c 2019.
260 1 ▼a Ann Arbor: ▼b ProQuest Dissertations & Theses, ▼c 2019.
300 ▼a 228 p.
500 ▼a Source: Dissertations Abstracts International, Volume: 81-04, Section: B.
500 ▼a Advisor: Raybould, Helen E.
5021 ▼a Thesis (Ph.D.)--University of California, Davis, 2019.
506 ▼a This item must not be sold to any third party vendors.
506 ▼a This item must not be added to any third party search indexes.
520 ▼a Numerous aspects of health and disease are modulated by the dynamic bidirectional communication occurring between host and microbes. As such, this field has attracted significant research efforts to better understand how these dynamic relationships work. In particular, elucidating specific mediators and target pathways of commensal microorganisms such as Bifidobacteria are important for utilizing Bifidobacteria as a therapeutic agent in human health. The aims of this dissertation are to understand how the commensal Bifidobacteria interacts with and contributes to host physiology by evaluating changes in inflammatory markers and homeostatic pathways along the gut-brain axis. First, a specific Bifidobacteria-produced metabolite is identified and its effects on intestinal epithelial cells are investigated. Second, a model of persistent Bifidobacterium sustained with 2'-FL in a mouse model is established. Third, the persistent Bifidobacterium mouse model is used to explore whether a persistent population of Bifidobacteria sustained by 2'-FL offers protection against inflammatory challenge. Fourth, Bifidobacteria metabolite ILA is assed for interaction with the nodose ganglion neurons of the vagus nerve, or the neural component of the gut-brain axis. This dissertation advances the field by identifying a specific Bifidobacteria produced metabolite that activates important homeostatic and cytoprotective pathways, and by establishing a model of persistent Bifidobacteria in mice which is protective against inflammatory challenge. Taken together, the results of this dissertation advance the understanding of host-commensal relationships for better informed therapeutics to target inflammatory conditions.
590 ▼a School code: 0029.
650 4 ▼a Biology.
690 ▼a 0306
71020 ▼a University of California, Davis. ▼b Molecular, Cellular and Integrative Physiology.
7730 ▼t Dissertations Abstracts International ▼g 81-04B.
773 ▼t Dissertation Abstract International
790 ▼a 0029
791 ▼a Ph.D.
792 ▼a 2019
793 ▼a English
85640 ▼u http://www.riss.kr/pdu/ddodLink.do?id=T15492808 ▼n KERIS ▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다.
980 ▼a 202002 ▼f 2020
990 ▼a ***1008102
991 ▼a E-BOOK