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Activation of inflammatory signaling...

Torok, Anastasia Mitchell.

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Activation of inflammatory signaling cascades in Helicobacter pylori infection through engagement of the Toll-like receptor 2 and Toll-like receptor 5.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Activation of inflammatory signaling cascades in Helicobacter pylori infection through engagement of the Toll-like receptor 2 and Toll-like receptor 5./
作者:	Torok, Anastasia Mitchell.
面頁冊數:	198 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-10, Section: B, page: 4981.
Contained By:	Dissertation Abstracts International65-10B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3149197
ISBN:	9780496091256

Activation of inflammatory signaling cascades in Helicobacter pylori infection through engagement of the Toll-like receptor 2 and Toll-like receptor 5.
Torok, Anastasia Mitchell.

Activation of inflammatory signaling cascades in Helicobacter pylori infection through engagement of the Toll-like receptor 2 and Toll-like receptor 5. - 198 p.

Source: Dissertation Abstracts International, Volume: 65-10, Section: B, page: 4981.

Thesis (Ph.D.)--University of Virginia, 2005.

Helicobacter pylori infection causes gastritis and has been strongly associated with duodenal and peptic ulcers, adenocarcinoma, and non-Hodgkin's and MALT lymphomas. Interleukin-8 (IL-8) is secreted from host cells in response to H. pylori, which attracts components of the innate and adaptive immune systems to the sites of infection and, as such, IL-8 is a major contributor to H. pylori disease. In vitro infections have indicated that activation of NF-kappaB, activator protein-1 (AP-1), and the mitogen-activated protein kinases (MAPKs) are required for optimal induction of IL-8 in response to H. pylori infection. In this study, we examined the contribution of the Toll-like receptors (TLRs) to the activation of NF-kappaB and the MAPKs and to the secretion of IL-8 from H. pylori-infected cells. We show that human gastric epithelial cell lines can express TLR2, TLR4, and TLR5. We show here that H. pylori is recognized by TLR2 and TLR5, but not by TLR4. Furthermore, we determined that H. pylori LPS and flagellin are H. pylori virulence factors recognized by TLR2 and TLR5, respectively. We demonstrate that TLR2 and TLR5 are receptors through which H. pylori activates signal transduction pathways that lead to enhanced activation of NF-kappaB and p38, and the phosphorylation of ATF2, a component of AP-1. The TLR2- and TLR5-dependent activation of these signaling pathways results in more IL-8 secretion from H. pylori-infected TLR2- and TLR5-expressing cells than from infected cells that do not express either receptor. Lastly, we show that TLR2/TLR5-dependent IL-8 secretion from H. pylori-infected cells requires p38 activity. As IL-8 is an important mediator of H. pylori inflammation in vivo, this TLR2/TLR5-dependent mechanism of IL-8 secretion may contribute to the gastritis and disease observed in human patients infected by H. pylori .

ISBN: 9780496091256Subjects--Topical Terms:

1017734
Biology, Microbiology.

Activation of inflammatory signaling cascades in Helicobacter pylori infection through engagement of the Toll-like receptor 2 and Toll-like receptor 5.
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