語系:
繁體中文
English
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
The function of the murine complemen...
~
Hollmann, Travis J.
FindBook
Google Book
Amazon
博客來
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock./
作者:
Hollmann, Travis J.
面頁冊數:
190 p.
附註:
Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1379.
Contained By:
Dissertation Abstracts International66-03B.
標題:
Health Sciences, Immunology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3168438
ISBN:
9780542042102
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock.
Hollmann, Travis J.
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock.
- 190 p.
Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1379.
Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2005.
The complement system functions as a major effector for both the innate and adaptive immune response. Activation of the complement cascade by either the classical, alternative, or lectin pathway promotes the proteolysis of C3 and C5 thereby generating C3a and C5a. Referred to as anaphylatoxins, the C3a and C5a peptides mediate biological effects upon binding to their respective receptors; C3a binds to the C3a receptor (C3aR) while C5a binds to the C5a receptor (C5aR, CD88). Both C3a and C5a are known for their broad proinflammatory effects. Elevated levels of both peptides have been isolated from patients with a variety of inflammatory diseases such as COPD, asthma, RA, SLE, and sepsis. Recent studies suggest that C5a is a critical component in the acquired neutrophil dysfunction, coagulopathy, and progressive multi-organ dysfunction characteristic of sepsis. The primary hypothesis of this dissertation was that preventing C3a-C3aR and C5a-C5aR mediated pro-inflammatory effects would improve survival in endotoxic, bacteremic and septic shock. To test this hypothesis, the murine C3aR and C5aR genes were disrupted. Following disruption of both the C3aR and C5aR genes, no abnormalities were identified other than the absence of their respective mRNA and protein. In models of both endotoxic and bacteremic shock, C3aR deficient mice suffered increased mortality when compared to their wild type littermates. C3aR deficient mice also had elevated circulating IL-1beta levels. Using a model of sepsis, C3aR deficient mice had a higher circulating concentration of IL-6 and decreased peritoneal inflammatory infiltration. While these results were unexpected, they support an emerging role for C3a in immunomodulation. In contrast, following endotoxic or bacteremic shock, C5aR deficient mice experienced increased survival, less hemoconcentration and less thrombocytopenia. It was later determined that C5a mediated histamine release significantly contributes to host morbidity and mortality in bacteremic shock. These studies provide evidence that C5a functions primarily as a proinflammatory molecule in models of endotoxic and bacteremic shock. In the same models, C3a-C3aR interactions suppress the inflammatory response and protect the host. Collectively, these results present in vivo evidence that C3a and C5a have divergent biological functions.
ISBN: 9780542042102Subjects--Topical Terms:
1017716
Health Sciences, Immunology.
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock.
LDR
:03327nmm 2200265 4500
001
1822756
005
20061128081308.5
008
130610s2005 eng d
020
$a
9780542042102
035
$a
(UnM)AAI3168438
035
$a
AAI3168438
040
$a
UnM
$c
UnM
100
1
$a
Hollmann, Travis J.
$3
1911887
245
1 4
$a
The function of the murine complement C3a and C5a anaphylatoxin receptors in endotoxemia, bacteremia and septic shock.
300
$a
190 p.
500
$a
Source: Dissertation Abstracts International, Volume: 66-03, Section: B, page: 1379.
500
$a
Supervisor: Rick A. Wetsel.
502
$a
Thesis (Ph.D.)--The University of Texas Graduate School of Biomedical Sciences at Houston, 2005.
520
$a
The complement system functions as a major effector for both the innate and adaptive immune response. Activation of the complement cascade by either the classical, alternative, or lectin pathway promotes the proteolysis of C3 and C5 thereby generating C3a and C5a. Referred to as anaphylatoxins, the C3a and C5a peptides mediate biological effects upon binding to their respective receptors; C3a binds to the C3a receptor (C3aR) while C5a binds to the C5a receptor (C5aR, CD88). Both C3a and C5a are known for their broad proinflammatory effects. Elevated levels of both peptides have been isolated from patients with a variety of inflammatory diseases such as COPD, asthma, RA, SLE, and sepsis. Recent studies suggest that C5a is a critical component in the acquired neutrophil dysfunction, coagulopathy, and progressive multi-organ dysfunction characteristic of sepsis. The primary hypothesis of this dissertation was that preventing C3a-C3aR and C5a-C5aR mediated pro-inflammatory effects would improve survival in endotoxic, bacteremic and septic shock. To test this hypothesis, the murine C3aR and C5aR genes were disrupted. Following disruption of both the C3aR and C5aR genes, no abnormalities were identified other than the absence of their respective mRNA and protein. In models of both endotoxic and bacteremic shock, C3aR deficient mice suffered increased mortality when compared to their wild type littermates. C3aR deficient mice also had elevated circulating IL-1beta levels. Using a model of sepsis, C3aR deficient mice had a higher circulating concentration of IL-6 and decreased peritoneal inflammatory infiltration. While these results were unexpected, they support an emerging role for C3a in immunomodulation. In contrast, following endotoxic or bacteremic shock, C5aR deficient mice experienced increased survival, less hemoconcentration and less thrombocytopenia. It was later determined that C5a mediated histamine release significantly contributes to host morbidity and mortality in bacteremic shock. These studies provide evidence that C5a functions primarily as a proinflammatory molecule in models of endotoxic and bacteremic shock. In the same models, C3a-C3aR interactions suppress the inflammatory response and protect the host. Collectively, these results present in vivo evidence that C3a and C5a have divergent biological functions.
590
$a
School code: 2034.
650
4
$a
Health Sciences, Immunology.
$3
1017716
690
$a
0982
710
2 0
$a
The University of Texas Graduate School of Biomedical Sciences at Houston.
$3
1019338
773
0
$t
Dissertation Abstracts International
$g
66-03B.
790
1 0
$a
Wetsel, Rick A.,
$e
advisor
790
$a
2034
791
$a
Ph.D.
792
$a
2005
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3168438
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9213619
電子資源
11.線上閱覽_V
電子書
EB
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入