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A Novel Microbial Source of Stochasticity in Microbiota-Driven Diseases.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	A Novel Microbial Source of Stochasticity in Microbiota-Driven Diseases./
作者:	Yang, Yi.
面頁冊數:	1 online resource (106 pages)
附註:	Source: Dissertations Abstracts International, Volume: 85-01, Section: B.
Contained By:	Dissertations Abstracts International85-01B.
標題:	Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30248660click for full text (PQDT)
ISBN:	9798379778804

A Novel Microbial Source of Stochasticity in Microbiota-Driven Diseases.
Yang, Yi.

A Novel Microbial Source of Stochasticity in Microbiota-Driven Diseases. - 1 online resource (106 pages)

Source: Dissertations Abstracts International, Volume: 85-01, Section: B.

Thesis (Ph.D.)--Yale University, 2023.

Includes bibliographical references

Gut commensals with the capacity to translocate across the intestinal barrier can drive the development of diverse immune-mediated diseases. However, the key factors that dictate bacterial translocation remain unclear. Recent studies have revealed that gut microbiota strains can adapt and evolve throughout the lifetime of the host, raising the possibility that changes in individual commensals themselves over time may impact their propensity to elicit inflammatory disease. Here we show that within-host evolution of the model gut pathobiont Enterococcus gallinarum facilitates bacterial translocation and initiation of chronic inflammation. Using a combination of in vivo experimental evolution and comparative genomics, we found that E. gallinarum diverges into independent lineages adapted to colonize either luminal or mucosal niches in the gut. Compared to ancestral and luminal E. gallinarum, mucosally-adapted strains evade detection and clearance by the immune system, exhibit increased translocation to and survival within the mesenteric lymph nodes and liver, and initiate inflammatory responses in the intestine and liver. Mechanistically, these changes in bacterial behavior are associated with non-synonymous mutations or indels in defined regulatory genes in E. gallinarum, altered microbial gene expression programs, and remodeled cell wall structures. By extending to other commensal species, we found that Lactobacillus reuteri also exhibited broadly similar patterns of divergent evolution and enhanced immune evasion in a monocolonization-based model of within-host evolution. Overall, these studies define within-host evolution as a critical regulator of commensal pathogenicity that provides a unique source of stochasticity in the development and progression of microbiota-driven disease.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2023

Mode of access: World Wide Web

ISBN: 9798379778804Subjects--Topical Terms:

611031
Immunology.
Subjects--Index Terms:

Bacterial pathogenicityIndex Terms--Genre/Form:

542853
Electronic books.

A Novel Microbial Source of Stochasticity in Microbiota-Driven Diseases.
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538 $a Mode of access: World Wide Web
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