상세정보
Export to Refworks부가기능
Factors That Contribute to Group B Streptococcus Colonization and Disease States
상세 프로파일
| 자료유형 | 학위논문 |
|---|---|
| 서명/저자사항 | Factors That Contribute to Group B Streptococcus Colonization and Disease States. |
| 개인저자 | Deng, Liwen . |
| 단체저자명 | University of California, San Diego. Biology (Joint Doctoral with SDSU). |
| 발행사항 | [S.l.]: University of California, San Diego., 2019. |
| 발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2019. |
| 형태사항 | 197 p. |
| 기본자료 저록 | Dissertations Abstracts International 81-05B. Dissertation Abstract International |
| ISBN | 9781392512944 |
| 학위논문주기 | Thesis (Ph.D.)--University of California, San Diego, 2019. |
| 일반주기 |
Source: Dissertations Abstracts International, Volume: 81-05, Section: B.
Includes supplementary digital materials. Advisor: Kelley, Scott |
| 이용제한사항 | This item must not be sold to any third party vendors.This item must not be added to any third party search indexes. |
| 요약 | Streptococcus agalactiae (Group B Streptococcus [GBS]) is an opportunistic pathogen that normally colonizes healthy adults asymptomatically and is a frequent inhabitant of the vaginal tract in women. However, GBS can cause severe disease when transmitted to newborns. Despite widespread antibiotic prophylaxis administration to colonized mothers, GBS remains a leading cause of neonatal meningitis. Bacterial meningitis is a life-threatening infection of the central nervous system (CNS) and is marked by GBS gaining access to the blood and further by penetration of GBS across the blood-brain barrier (BBB) and activation of host inflammatory responses. Although several GBS surface proteins have been shown to impact bacterial adhesion to endothelium, a direct interaction between a GBS factor and a host endothelial ligand had not been described. Additionally, while it is known that the bacterium tightly regulates its expression of virulence factors in order to occupy various host niches, there are currently many uncharacterized GBS transcriptional regulators. Also, GBS likely competes or cooperates with other resident microbes in the vaginal tract during colonization, however little work has been done to model polymicrobial interactions within this host niche. For this PhD dissertation, I investigated how this bacterium is able to persist in the vagina, transition to an invasive pathogen, disrupt host barriers, and ultimately penetrate into the brain to cause meningitis. I examined a GBS adhesin which promoted bacterial attachment to the brain endothelium and discovered the endothelial receptor for this GBS factor. I also characterized a GBS transcriptional regulator that influenced meningitis as well as GBS vaginal carriage by impacting host immune signaling. Lastly, I developed an in vivo vaginal colonization model for another common opportunistic pathogen, Staphylococcus aureus, which likely interacts with GBS within this host niche. Using this model, I showed that bacterial interactions with fibrinogen as well as iron uptake are key determinants of vaginal persistence. Taken together, this dissertation furthers our understanding of how GBS adapts to different host niches in order to transition from asymptomatic colonization to causing invasive inflammatory disease and provides novel insights into GBS disease pathogenesis and treatment strategies to prevent colonization and invasive CNS disease. |
| 일반주제명 | Biology. |
| 언어 | 영어 |
| 바로가기 | 
: 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |
