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Modulation of airway responses to an...

Allakhverdieva, Zoulfia.

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Modulation of airway responses to antigen in a rat model of allergic asthma.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Modulation of airway responses to antigen in a rat model of allergic asthma./
作者:	Allakhverdieva, Zoulfia.
面頁冊數:	260 p.
附註:	Source: Dissertation Abstracts International, Volume: 63-10, Section: B, page: 4576.
Contained By:	Dissertation Abstracts International63-10B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NQ73468
ISBN:	0612734684

Modulation of airway responses to antigen in a rat model of allergic asthma.
Allakhverdieva, Zoulfia.

Modulation of airway responses to antigen in a rat model of allergic asthma. - 260 p.

Source: Dissertation Abstracts International, Volume: 63-10, Section: B, page: 4576.

Thesis (Ph.D.)--Universite de Montreal (Canada), 2002.

Airway obstruction, hyperresponsiveness and the accumulation and persistence within the airways of inflammatory cells characterize asthma. There is substantial evidence of lymphocyte activation and cytokine over-expression in both human subjects with asthma and animals undergoing airway challenge with a sensitizing antigen. We have previously shown in sensitized Sprague-Dawley (SD) rats that depletion of CD8+ cells caused an increase in the late airway response (LAR) and cellular infiltration after antigen challenge. To better delineate the mechanism of CD8+ cell involvement in the development of the LAR and airway inflammation, we investigated the pattern of chemokine and cytokine production after antigen challenge.

ISBN: 0612734684Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Modulation of airway responses to antigen in a rat model of allergic asthma.
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245 1 0 $a Modulation of airway responses to antigen in a rat model of allergic asthma.
300 $a 260 p.
500 $a Source: Dissertation Abstracts International, Volume: 63-10, Section: B, page: 4576.
500 $a Adviser: Paolo M. Renzi.
502 $a Thesis (Ph.D.)--Universite de Montreal (Canada), 2002.
520 $a Airway obstruction, hyperresponsiveness and the accumulation and persistence within the airways of inflammatory cells characterize asthma. There is substantial evidence of lymphocyte activation and cytokine over-expression in both human subjects with asthma and animals undergoing airway challenge with a sensitizing antigen. We have previously shown in sensitized Sprague-Dawley (SD) rats that depletion of CD8+ cells caused an increase in the late airway response (LAR) and cellular infiltration after antigen challenge. To better delineate the mechanism of CD8+ cell involvement in the development of the LAR and airway inflammation, we investigated the pattern of chemokine and cytokine production after antigen challenge.
520 $a As previously reported, CD8-depletion before antigen challenge led to a significant enhancement of the LAR in SD rats, that usually do not develop LAR after sensitization and antigen challenge. CD8-depletion also caused an enhancement of the inflammatory response and an accumulation of a large number of eosinophils in the airways. In addition, there was an increase in eotaxin, a downregulation of IFNgamma mRNA, and no detectable effect on IL-4, IL-5, RANTES, and MCP-1 mRNA expression in CD8-depleted rats after ovalbumin (OVA) challenge. Thus, CD8+ cells appear to exert their effects through decreased production of eotaxin and increased production of IFN-gamma mRNA.
520 $a The presence of eosinophils in affected tissues is one of the hallmarks of allergic inflammation. Tissue eosinophilia is probably due to a combination of several rather specific and coordinated cellular processes appearing at different stages that include adhesion, chemotaxis, and activation. IL-3, IL-5 and GM-CSF are amongst several cytokines that have been shown to be increased in asthma and to contribute to atopic inflammation. They mediate their effect via receptors that have a common beta subunit (betac). Eotaxin, a potent chemoattractant for eosinophils, acts via its specific receptor CCR3. CCR3 is primarily found on eosinophils and appears to play an important role in regulating the migration of these cells. The purpose of the following studies was to determine whether blocking the major pathways involved in eosinophil differentiation, recruitment, activation and survival would affect the airway responses after antigen challenge in Brown Norway (BN) rats, an allergic model of asthma. In order to block these pathways we employed phosphorothioate antisense oligonucleotides directed against receptors for these pathways.
520 $a Treatment of OVA-sensitized BN rats with intra-tracheal antisense oligonucleotides (AS-ODNs) directed against either the common betac or CCR3 significantly reduced lung betac and CCR3 mRNA and their respective protein expressions. Experimentally induced eosinophilia in OVA-sensitized AS-treated BN rats after antigen challenge was significantly decreased (**p < 0.01). Furthermore, when compared to control and mismatch ODN treated rats, beta c and CCR3 AS-ODNs caused inhibition of antigen-induced airway hyperresponsiveness to leukotriene D4 (LTD4). Taken together, our findings demonstrate that betac and CCR3 play important roles in the modulation of airway allergic responses after antigen challenge.
520 $a Understanding the mechanisms of eosinophil recruitment to the airways, and targeting pathways critical for regulation of eosinophil chemotaxis, activation and survival, will aid in the development of new anti-inflammatory agents for the treatment of asthma.
590 $a School code: 0992.
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0982
710 2 0 $a Universite de Montreal (Canada). $3 1018132
773 0 $t Dissertation Abstracts International $g 63-10B.
790 1 0 $a Renzi, Paolo M., $e advisor
790 $a 0992
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NQ73468