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LEADER 04311ctm 2200685 i 4500

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003 OCoLC;

005 20260519124538.0;

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035 a| (OCoLC)166352287;

050 4 a| RC591b| .W96 2005;

049 a| EREE;

100 1 a| Wynne, Brandi M.,e| author.;

245 10 a| Differential expression of genes under conditions dissociating airway inflammation and hyperresponsiveness in a murine model of allergic asthma /c| by Brandi M. Wynne.;

264 0 c| 2005.;

300 a| 57 leaves :b| illustrations (some color) ;c| 28 cm;

336 a| textb| txt2| rdacontent;

337 a| unmediatedb| n2| rdamedia;

338 a| volumeb| nc2| rdacarrier;

502 b| M.S.c| East Carolina Universityd| 2005;

500 a| Presented to the faculty of the Department of Biology.;

500 a| Advisor: Michael R. VanScott;

500 a| Advisor: Gerhard W. Kalmus;

520 3 a| Airway hyperresponsiveness in allergic asthma is thought to be a result of eosinophilic inflammation. However, data on the anti-inflammatory cytokine IL-10 suggest an independent model of airway hyperresponsiveness, separate from inflammatory mechanisms . In wild type mice, IL-10 attenuates allergic inflammation and knockout of the IL-10 gene has an opposite effect. However, IL-10 has an opposite effect on airway hyperresponsiveness. VanScott and co-workers showed that treating wild type mice with IL-10 augments airway hyperresponsiveness. Conversely, knockout of the IL-10 gene attenuates hyperresponsiveness. In this study, microarray analysis was used to compare gene expression in wild type and IL-10 KO mice to identify molecular targets that are uniquely expressed under conditions where airway hyperresponsiveness is observed, but inflammation is minimal. Wild-type and IL-10 KO C57/B16 mice were sensitized and challenged with ragweed and then treated with either saline or recombinant human IL-10. Airway hyperresponsiveness was confirmed by whole body plethysmography, trachea and lung tissues was harvested, and total RNA was obtained for the microarray analysis. A total of 29 genes were identified as being uniquely expressed in association with airway hyperresponsiveness. One gene, Rhognef, was of particular interest in this laboratory, and was further explored using Real Time PCR.;

504 a| Includes bibliographical references (leaves 52-57).;

650 0 a| Asthmax| Research.;

650 0 a| Airway (Medicine);

650 0 a| Inflammation.;

650 0 a| Gene expression.;

650 0 a| Eosinophils.;

650 0 a| Cytokines.;

650 0 a| Mice as laboratory animals.;

650 2 a| Inflammation0| (DNLM)D007249;

650 2 a| Gene Expression0| (DNLM)D015870;

650 2 a| Eosinophils0| (DNLM)D004804;

650 2 a| Cytokines0| (DNLM)D016207;

650 7 a| Airway (Medicine)2| fast0| (OCoLC)fst00803879;

650 7 a| Asthmax| Research.2| fast0| (OCoLC)fst00819327;

650 7 a| Cytokines.2| fast0| (OCoLC)fst00886268;

650 7 a| Eosinophils.2| fast0| (OCoLC)fst00913652;

650 7 a| Gene expression.2| fast0| (OCoLC)fst00939613;

650 7 a| Inflammation.2| fast0| (OCoLC)fst00972432;

650 7 a| Mice as laboratory animals.2| fast0| (OCoLC)fst01019388;

655 2 a| Academic Dissertation0| (DNLM)D019478;

655 7 a| Academic theses.2| fast0| (OCoLC)fst01726453;

655 7 a| Academic theses.2| lcgft;

655 7 a| Thèses et écrits académiques.2| rvmgf0| (CaQQLa)RVMGF-000001173;

700 1 a| Van Scott, Michael R.,e| degree supervisor.;

700 1 a| Kalmus, Gerhard W.,e| degree supervisor.;

710 2 a| East Carolina University.b| Department of Biology.;

856 41 z| Access via ScholarShipu| http://hdl.handle.net/10342/12935;

949 a| Click on web addressw| asish| joyner101;

949 a| Click on web addressw| asish| hsl111;

994 a| C0b| ERE;

596 a| 1 4;

998 a| 1091212;

999 a| ASK AT SPECIAL COLLECTIONS DESKw| ASISc| 1i| MQ1933753l| JSCJTHDm| JOYNERr| Ys| Yt| JSCJTHDu| 8/28/2007x| ETDz| JSPECCOLLo| .STAFF. 0;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 1091212-4001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 5/19/2026x| ETDz| JERESOURCE;

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Differential expression of genes under conditions dissociating airway inflammation and hyperresponsiveness in a murine model of allergic asthma / by Brandi M. Wynne.

Author/creator	Wynne, Brandi M. author.
Other author	Van Scott, Michael R., degree supervisor.
Other author	Kalmus, Gerhard W., degree supervisor.
Other author	East Carolina University. Department of Biology.
Format	Theses and dissertations
Production	2005.
Description	57 leaves : illustrations (some color) ; 28 cm
Supplemental Content	Access via ScholarShip
Subjects	Asthma--Research. Airway (Medicine) Inflammation. Gene expression. Eosinophils. Cytokines. Mice as laboratory animals. Inflammation Gene Expression Eosinophils Cytokines

Summary	Airway hyperresponsiveness in allergic asthma is thought to be a result of eosinophilic inflammation. However, data on the anti-inflammatory cytokine IL-10 suggest an independent model of airway hyperresponsiveness, separate from inflammatory mechanisms . In wild type mice, IL-10 attenuates allergic inflammation and knockout of the IL-10 gene has an opposite effect. However, IL-10 has an opposite effect on airway hyperresponsiveness. VanScott and co-workers showed that treating wild type mice with IL-10 augments airway hyperresponsiveness. Conversely, knockout of the IL-10 gene attenuates hyperresponsiveness. In this study, microarray analysis was used to compare gene expression in wild type and IL-10 KO mice to identify molecular targets that are uniquely expressed under conditions where airway hyperresponsiveness is observed, but inflammation is minimal. Wild-type and IL-10 KO C57/B16 mice were sensitized and challenged with ragweed and then treated with either saline or recombinant human IL-10. Airway hyperresponsiveness was confirmed by whole body plethysmography, trachea and lung tissues was harvested, and total RNA was obtained for the microarray analysis. A total of 29 genes were identified as being uniquely expressed in association with airway hyperresponsiveness. One gene, Rhognef, was of particular interest in this laboratory, and was further explored using Real Time PCR.
General note	Presented to the faculty of the Department of Biology.
General note	Advisor: Michael R. VanScott
General note	Advisor: Gerhard W. Kalmus
Dissertation note	M.S. East Carolina University 2005
Bibliography note	Includes bibliographical references (leaves 52-57).
Genre/form	Academic theses.
Genre/form	Academic theses.
Genre/form	Thèses et écrits académiques.

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Differential expression of genes under conditions dissociating airway inflammation and hyperresponsiveness in a murine model of allergic asthma / by Brandi M. Wynne.

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