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Interleukin-17 signaling: Target ge...

Ruddy, Matthew J.

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Interleukin-17 signaling: Target genes and role in periodontal disease.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Interleukin-17 signaling: Target genes and role in periodontal disease./
作者:	Ruddy, Matthew J.
面頁冊數:	142 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-08, Section: B, page: 3939.
Contained By:	Dissertation Abstracts International65-08B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3141311
ISBN:	0496884433

Interleukin-17 signaling: Target genes and role in periodontal disease.
Ruddy, Matthew J.

Interleukin-17 signaling: Target genes and role in periodontal disease. - 142 p.

Source: Dissertation Abstracts International, Volume: 65-08, Section: B, page: 3939.

Thesis (Ph.D.)--State University of New York at Buffalo, 2004.

IL-17 is the founding member of an emerging family of inflammatory cytokines whose functions remain poorly defined. This work describes two lines of investigation to determine the function of IL-17 in bone: in vitro using a cell culture system in a preosteoblast cell line, and in vivo using IL-17 receptor knockout mice.

ISBN: 0496884433Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Interleukin-17 signaling: Target genes and role in periodontal disease.
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520 $a IL-17 is the founding member of an emerging family of inflammatory cytokines whose functions remain poorly defined. This work describes two lines of investigation to determine the function of IL-17 in bone: in vitro using a cell culture system in a preosteoblast cell line, and in vivo using IL-17 receptor knockout mice.
520 $a IL-17 amplifies inflammatory responses by triggering production of pro-inflammatory mediators including IL-6, IL-8, and TNFalpha. In the pre-osteoblast line MC3T3-E1, IL-17 synergizes potently with suboptimal doses of TNFalpha to produce IL-6. In investigating the molecular mechanism underlying synergy between TNFalpha and IL-17 signaling, we found that Affymetrix microarray experiments comparing genes induced by TNFalpha versus IL-17+TNFalpha revealed differential expression of the transcription factor C/EBPdelta. We then showed C/EBPdelta expression is at least partially responsible for mediating the synergistic production of IL-6. Another novel target gene identified in our microarray analysis was the LPS-inducible CXC chemokine LIX. We demonstrated that IL-17+TNFalpha resulted in a LIX specific induction of neutrophil migration, suggesting another molecular mechanism by which IL-17 modulates neutrophil trafficking and inflammation.
520 $a To examine the function of IL-17R signaling on bone metabolism in vivo, we used a model of infection-induced bone loss in IL-17R-/- mice. Specifically, mice infected with the periodontal pathogen P. gingivalis (Pg) experience bone loss in the alveolar bone crest of the jaw. As previously reported, our results indicate that both male and female wild type C57BL/6J mice were fairly resistant to P. gingivalis-induced alveolar bone loss. However, female mice deficient in the IL-17R are more susceptible to alveolar bone loss than their wild type counterparts following P. gingivalis infection. This suggests that the IL-17R acts predominantly in vivo to defend the host against periodontal infection and subsequent alveolar bone loss.
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