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An Antibiotic-Perturbed Microbiota in Early Life Has Long-Lasting Consequences on the Gut Microbial Community and Host Health in Two Murine Models of Disease- [electronic resource]
An Antibiotic-Perturbed Microbiota in Early Life Has Long-Lasting Consequences on the Gut Microbial Community and Host Health in Two Murine Models of Disease- [electronic resource]
상세정보
- 자료유형
- 학위논문(국외)
- 자관 청구기호
- 기본표목-개인명
- 표제와 책임표시사항
- An Antibiotic-Perturbed Microbiota in Early Life Has Long-Lasting Consequences on the Gut Microbial Community and Host Health in Two Murine Models of Disease - [electronic resource] / Schulfer, Anjelique F.
- 발행, 배포, 간사 사항
- 발행, 배포, 간사 사항
- 형태사항
- 1 online resource(193 p)
- 일반주기
- Source: Dissertation Abstracts International, Volume: 78-12(E), Section: B.
- 일반주기
- Adviser: Martin J. Blaser.
- 학위논문주기
- Thesis (Ph.D.)--New York University, 2017.
- 요약 등 주기
- 요약Antibiotic use, especially amongst children, is associated with an increased risk of developing obesity, asthma, and inflammatory bowel disease (IBD) later in life. As we reach a greater understanding of the role of the gut microbiota in disease development, it is becoming clear that antibiotic-induced changes to the gut microbiota are likely key mediators of this increased risk. We investigated the role of an antibiotic-altered gut microbiota in two major murine models. First, we hypothesized that cohousing antibiotic-exposed and control mice would change the gut microbiota and the rate of weight gain later in life. We gave C57BL/6J mice subtherapeutic antibiotic treatment (STAT) or not (Control) for the first 4 weeks of life. STAT mice gained weight faster than Control, especially after introduction of high fat diet (HFD). After the antibiotic exposure ended at 4 weeks, we cohoused STAT and Control mice. Cohoused mice had an altered gut microbiota and gained weight faster than STAT mice in response to HFD. In the second model, we hypothesized that an antibiotic-perturbed microbiota would accelerate colitis in a genetically susceptible mouse. We colonized germ-free pregnant C57BL/6J mice (either WT or IL10--/--) with either STAT or Control gut microbiota. Mice born to IL10--/-- mothers that had received the STAT microbiota had an increased risk of developing colitis by the time they reached 21 weeks of age. In both models we characterized changes in the gut microbiota community composition over time and identified taxa that may be responsible for the disease outcome and are strong targets for future studies. This work demonstrates that the gut microbiota can be therapeutically targeted after early-life antibiotic exposure to change the risk of accelerated weight gain, that consequences of antibiotic use on the microbiota can be transferred between generations, and that an antibiotic-altered microbiota can accelerate the onset of colitis in genetically susceptible hosts.
- 주제명부출표목-일반주제명
- 주제명부출표목-일반주제명
- 주제명부출표목-일반주제명
- 부출표목-단체명
- 기본자료저록
- Dissertation Abstracts International. 78-12B(E).
- 기본자료저록
- Dissertation Abstract International
- 전자적 위치 및 접속
- 원문정보보기
- 소장사항
-
20180515 2018
MARC
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■00520180518093528
■007cr
■020 ▼a9780355127645
■035 ▼a(MiAaPQ)AAI10258322
■035 ▼a(MiAaPQ)nyu:12846
■040 ▼aMiAaPQ▼cMiAaPQ
■090 ▼a전자도서(박사논문)
■1001 ▼aSchulfer, Anjelique F.
■24513▼aAn Antibiotic-Perturbed Microbiota in Early Life Has Long-Lasting Consequences on the Gut Microbial Community and Host Health in Two Murine Models of Disease▼h[electronic resource]▼cSchulfer, Anjelique F.
■260 ▼a[Sl]▼bNew York University▼c2017
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2017
■300 ▼a1 online resource(193 p)
■500 ▼aSource: Dissertation Abstracts International, Volume: 78-12(E), Section: B.
■500 ▼aAdviser: Martin J. Blaser.
■5021 ▼aThesis (Ph.D.)--New York University, 2017.
■520 ▼aAntibiotic use, especially amongst children, is associated with an increased risk of developing obesity, asthma, and inflammatory bowel disease (IBD) later in life. As we reach a greater understanding of the role of the gut microbiota in disease development, it is becoming clear that antibiotic-induced changes to the gut microbiota are likely key mediators of this increased risk. We investigated the role of an antibiotic-altered gut microbiota in two major murine models. First, we hypothesized that cohousing antibiotic-exposed and control mice would change the gut microbiota and the rate of weight gain later in life. We gave C57BL/6J mice subtherapeutic antibiotic treatment (STAT) or not (Control) for the first 4 weeks of life. STAT mice gained weight faster than Control, especially after introduction of high fat diet (HFD). After the antibiotic exposure ended at 4 weeks, we cohoused STAT and Control mice. Cohoused mice had an altered gut microbiota and gained weight faster than STAT mice in response to HFD. In the second model, we hypothesized that an antibiotic-perturbed microbiota would accelerate colitis in a genetically susceptible mouse. We colonized germ-free pregnant C57BL/6J mice (either WT or IL10--/--) with either STAT or Control gut microbiota. Mice born to IL10--/-- mothers that had received the STAT microbiota had an increased risk of developing colitis by the time they reached 21 weeks of age. In both models we characterized changes in the gut microbiota community composition over time and identified taxa that may be responsible for the disease outcome and are strong targets for future studies. This work demonstrates that the gut microbiota can be therapeutically targeted after early-life antibiotic exposure to change the risk of accelerated weight gain, that consequences of antibiotic use on the microbiota can be transferred between generations, and that an antibiotic-altered microbiota can accelerate the onset of colitis in genetically susceptible hosts.
■590 ▼aSchool code: 0146.
■650 4▼aHealth sciences
■650 4▼aMicrobiology
■650 4▼aMedicine
■690 ▼a0566
■690 ▼a0410
■690 ▼a0564
■71020▼aNew York University▼bBasic Medical Science.
■7730 ▼tDissertation Abstracts International▼g78-12B(E).
■773 ▼tDissertation Abstract International
■790 ▼a0146
■791 ▼aPh.D.
■792 ▼a2017
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T14822273▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
■980 ▼a20180515▼f2018
