東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

FindBook

Google Book

Amazon

博客來

Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague./
作者:	Crane, Samantha Danielle.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
面頁冊數:	156 p.
附註:	Source: Dissertations Abstracts International, Volume: 83-03, Section: B.
Contained By:	Dissertations Abstracts International83-03B.
標題:	Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28650675
ISBN:	9798538109968

Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague.
Crane, Samantha Danielle.

Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 156 p.

Source: Dissertations Abstracts International, Volume: 83-03, Section: B.

Thesis (Ph.D.)--University of Arkansas for Medical Sciences, 2021.

This item must not be sold to any third party vendors.

Yersinia pestis is a lethal pathogen and the causative agent of plague. Pneumonic plague results in 100% mortality within seven days without antibiotic intervention and is caused by inhalation of infected aerosols or respiratory droplets. Because of its lethality and ease of transmission, Y. pestis is classified as a CDC Tier I Select Agent and a NIAID Category A Priority Pathogen as it poses severe risks to public health and national security. The progression of pneumonic plague occurs via pre-inflammatory and pro-inflammatory phases of disease. Upon intranasal inoculation of mice with Y. pestis, the pre-inflammatory phase begins, and is characterized by rapid bacterial growth in the lungs without invoking a substantial immune response. Between 36-48 hours post-infection (hpi), the disease shifts to the pro-inflammatory phase in which influx of neutrophils and overzealous pro-inflammatory host responses occur, resulting in fatal pneumonia by 72 hpi. Despite Y. pestis' lethality and status as a priority pathogen, a number of questions remain regarding the bacterial and host determinants contributing to disease progression. The work presented herein serves to characterize bacterial and host factors contributing to pneumonic plague lethality. In the first work, we investigate the role of a novel Y. pestis virulence factor, BipA. We show that BipA is involved in the response to antimicrobial peptide challenge and Y. pestis adherence to macrophage and alveolar epithelial cells in vitro. We show that BipA confers resistance to neutrophil-mediated killing and promotes survival of Y. pestis during the pre-inflammatory phase of disease to promote infection. In the second work, we identify host responses associated with decreased lung pathology and enhanced murine survival of pneumonic plague. Administration of fluticasone propionate prior to and during the course of pneumonic plague with delayed antibiotic administration that is otherwise ineffective increased murine survival and revealed altered host responses that may contribute to plague lethality. Together, this dissertation adds to understanding of bacterial and host factors contributing to progression of primary pneumonic plague.

ISBN: 9798538109968Subjects--Topical Terms:

536250
Microbiology.
Subjects--Index Terms:

Bacterial pathogenesis

Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague.
LDR:03472nmm a2200397 4500 001 2346243
005 20220620110454.5
008 241004s2021 ||||||||||||||||| ||eng d
020 $a 9798538109968
035 $a (MiAaPQ)AAI28650675
035 $a AAI28650675
040 $a MiAaPQ $c MiAaPQ
100 1 $a Crane, Samantha Danielle. $3 3685313
245 1 0 $a Characterization of Bacterial and Host Factors Contributing to Progression of Primary Pneumonic Plague.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2021
300 $a 156 p.
500 $a Source: Dissertations Abstracts International, Volume: 83-03, Section: B.
500 $a Advisor: Pechous, Roger.
502 $a Thesis (Ph.D.)--University of Arkansas for Medical Sciences, 2021.
506 $a This item must not be sold to any third party vendors.
520 $a Yersinia pestis is a lethal pathogen and the causative agent of plague. Pneumonic plague results in 100% mortality within seven days without antibiotic intervention and is caused by inhalation of infected aerosols or respiratory droplets. Because of its lethality and ease of transmission, Y. pestis is classified as a CDC Tier I Select Agent and a NIAID Category A Priority Pathogen as it poses severe risks to public health and national security. The progression of pneumonic plague occurs via pre-inflammatory and pro-inflammatory phases of disease. Upon intranasal inoculation of mice with Y. pestis, the pre-inflammatory phase begins, and is characterized by rapid bacterial growth in the lungs without invoking a substantial immune response. Between 36-48 hours post-infection (hpi), the disease shifts to the pro-inflammatory phase in which influx of neutrophils and overzealous pro-inflammatory host responses occur, resulting in fatal pneumonia by 72 hpi. Despite Y. pestis' lethality and status as a priority pathogen, a number of questions remain regarding the bacterial and host determinants contributing to disease progression. The work presented herein serves to characterize bacterial and host factors contributing to pneumonic plague lethality. In the first work, we investigate the role of a novel Y. pestis virulence factor, BipA. We show that BipA is involved in the response to antimicrobial peptide challenge and Y. pestis adherence to macrophage and alveolar epithelial cells in vitro. We show that BipA confers resistance to neutrophil-mediated killing and promotes survival of Y. pestis during the pre-inflammatory phase of disease to promote infection. In the second work, we identify host responses associated with decreased lung pathology and enhanced murine survival of pneumonic plague. Administration of fluticasone propionate prior to and during the course of pneumonic plague with delayed antibiotic administration that is otherwise ineffective increased murine survival and revealed altered host responses that may contribute to plague lethality. Together, this dissertation adds to understanding of bacterial and host factors contributing to progression of primary pneumonic plague.
590 $a School code: 0365.
650 4 $a Microbiology. $3 536250
650 4 $a Immunology. $3 611031
650 4 $a Infections. $3 1621997
650 4 $a Pathogens. $3 3540520
650 4 $a Epidemiology. $3 568544
650 4 $a Disease. $3 705846
650 4 $a Bacteria. $3 550366
650 4 $a Aerosols. $3 671355
650 4 $a Fever. $3 3444643
650 4 $a Peptides. $3 605772
650 4 $a Kinases. $3 3558077
650 4 $a Proteins. $3 558769
650 4 $a Antibiotics. $3 670318
650 4 $a Pandemics. $3 3464080
650 4 $a Epidemics. $3 588395
650 4 $a Public health. $3 534748
650 4 $a Antimicrobial agents. $3 3556833
650 4 $a Bone marrow. $3 1621080
650 4 $a Antigens. $3 700737
650 4 $a Pathogenesis. $3 3561735
653 $a Bacterial pathogenesis
653 $a BipA
653 $a Fluticasone propionate
653 $a Pneumonia
653 $a Pneumonic plague
653 $a Yersinia pestis
690 $a 0410
690 $a 0982
690 $a 0573
690 $a 0766
710 2 $a University of Arkansas for Medical Sciences. $b Microbiology and Immunology. $3 3182995
773 0 $t Dissertations Abstracts International $g 83-03B.
790 $a 0365
791 $a Ph.D.
792 $a 2021
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28650675