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Cytokine regulation of CC chemokine ...

Cheng, Sara S.

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Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells./
Author:	Cheng, Sara S.
Description:	117 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0521.
Contained By:	Dissertation Abstracts International65-02B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3121904
ISBN:	049669255X

Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells.
Cheng, Sara S.

Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells. - 117 p.

Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0521.

Thesis (Ph.D.)--University of Michigan, 2004.

Chemokines and chemokine receptors play an important role in leukocyte trafficking. Many environmental factors can influence the progression of inflammatory processes by modulating chemokine receptor expression on specific cell types. This thesis has investigated the regulation of CC-type chemokine receptors on human neutrophils and endothelial cells. A variety of in vitro methods were used including tissue culture, ribonuclease protection, flow cytometry, ELISA, and microchamber chemotaxis assays, as well as an in vivo murine model of acute inflammation. It was found that stimulated neutrophils and endothelial cells express chemokine receptors that are absent on cells in the unstimulated state, and that these newly expressed receptors mediate novel effects on cellular function.

ISBN: 049669255XSubjects--Topical Terms:

1017686
Biology, Cell.

Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells.
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020 $a 049669255X
035 $a (UnM)AAI3121904
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040 $a UnM $c UnM
100 1 $a Cheng, Sara S. $3 1928634
245 1 0 $a Cytokine regulation of CC chemokine receptors on human neutrophils and endothelial cells.
300 $a 117 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0521.
500 $a Chair: Steven L. Kunkel.
502 $a Thesis (Ph.D.)--University of Michigan, 2004.
520 $a Chemokines and chemokine receptors play an important role in leukocyte trafficking. Many environmental factors can influence the progression of inflammatory processes by modulating chemokine receptor expression on specific cell types. This thesis has investigated the regulation of CC-type chemokine receptors on human neutrophils and endothelial cells. A variety of in vitro methods were used including tissue culture, ribonuclease protection, flow cytometry, ELISA, and microchamber chemotaxis assays, as well as an in vivo murine model of acute inflammation. It was found that stimulated neutrophils and endothelial cells express chemokine receptors that are absent on cells in the unstimulated state, and that these newly expressed receptors mediate novel effects on cellular function.
520 $a Chapter 2 documents experiments showing that neutrophils stimulated with granulocyte-macrophage colony stimulating factor (GM-CSF) upregulate the receptor CCR1 and become functionally responsive to CCR1 ligands in vitro. Chapter 3 contains evidence that TNF-alpha stimulation of endothelial cells upregulates CCR3 expression. Furthermore, the CCR3 ligand eotaxin (CXCL11) suppresses TNF-alpha-induced IL-8 (CXCL-8) production, an effect partially mediated by an acceleration of IL-8 mRNA degradation. This effect was specific for IL-8 in that it did not affect production of other chemokines tested, and was mediated by G-protein and phosphatidyl-inositol 3-kinase (PI3K). These findings were quite interesting, since IL-8 is a well-characterized potent neutrophil chemoattractant. We hypothesized that eotaxin might suppress neutrophil recruitment in vivo via downregulation of neutrophil-specific chemokines. In Chapter 4, we present evidence that mice that are deficient in eotaxin, either through genetic deletion of the eotaxin gene or through immunodepletion of eotaxin protein, have increased neutrophil recruitment to peripheral sites during endotoxemia. Furthermore, treatment of eotaxin knockout mice with recombinant murine eotaxin resulted in decreased neutrophil recruitment. These findings were consistent with the hypothesis generated by the data provided in Chapter 3.
520 $a In summary, this thesis project has shown that cytokine modulation of CC chemokine receptor expression on neutrophils and endothelial cells has important functional consequences on the inflammatory capacity of these cell types. This work contributes substantially to our understanding of the dynamic nature of chemokine networking during inflammation.
590 $a School code: 0127.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0379
690 $a 0982
690 $a 0433
710 2 0 $a University of Michigan. $3 777416
773 0 $t Dissertation Abstracts International $g 65-02B.
790 1 0 $a Kunkel, Steven L., $e advisor
790 $a 0127
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3121904