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Microarray analysis of PBMC gene exp...

Hu, Wanchung John.

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Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection./
作者:	Hu, Wanchung John.
面頁冊數:	227 p.
附註:	Adviser: August Louis Bourgeois.
Contained By:	Dissertation Abstracts International68-11B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288472
ISBN:	9780549312383

Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection.
Hu, Wanchung John.

Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection. - 227 p.

Adviser: August Louis Bourgeois.

Thesis (Ph.D.)--The Johns Hopkins University, 2008.

Hypothesis/theory. Gene expression profiles of peripheral blood mononuclear cells (PBMCs) will change after malarial infection and these changes are related to the pathogenesis and immunity of malaria.

ISBN: 9780549312383Subjects--Topical Terms:

1017730
Biology, Genetics.

Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection.
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100 1 $a Hu, Wanchung John. $3 1267745
245 1 0 $a Microarray analysis of PBMC gene expression profiles after Plasmodium falciparum malarial infection.
300 $a 227 p.
500 $a Adviser: August Louis Bourgeois.
500 $a Source: Dissertation Abstracts International, Volume: 68-11, Section: B, page: 7232.
502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2008.
520 $a Hypothesis/theory. Gene expression profiles of peripheral blood mononuclear cells (PBMCs) will change after malarial infection and these changes are related to the pathogenesis and immunity of malaria.
520 $a Methods. PBMCs were collected from 15 falciparum malaria infected Cameroonian adults during acute infection and during the remission period. PBMCs were also collected from 22 healthy U.S. volunteers prior to experimental infection with P. falciparum and again during the early stage of their illness. Microarray analysis was used to study gene expression profiles in these PBMCs.
520 $a Results. First, common and divergent immune response signaling pathways were identified in PBMC in early and acute febrile malaria. The results showed up-regulation of TLR signaling, NFkB, TNF-alpha, IL1-beta, IFN-gamma, IRF1, and MHC class I & II molecules during both early and acute febrile malaria. P38 MAPK related genes and apoptosisrelated genes were up-regulated in acute febrile malaria but un-changed in early malaria.
520 $a In subsequent studies, expression levels for genes potentially related to the pathogenesis of P. falciparum malaria were examined. In early or acute malaria, CD36, ICAM1, coagulation-related genes (SERPINB2, thrombomudulin, thrombospondin), heat shock proteins, glycolytic enzymes, glucose transporters, and H+-ATPases were up-regulated. Heat shock protein and IL-1beta expression levels were higher in those subjects with the most significant febrile response; while high MafB gene expression levels were negatively correlated with hemoglobin and platelet counts. Up-regulation of CD36, ICAM1, thrombospondin, and thrombomodulin gene expression levels may contribute to the pathogenesis of cerebral malaria. Glycolytic enzymes, glucose transporters, and H+-ATPases may also contribute to the metabolic acidosis and hypoglycemia frequently associated with malarial infection.
520 $a Finally, gene expression levels for genes modulating host immune responses to P. falciparum were further examined. In early and acute malaria, interferon genes (for alpha/beta and gamma-interferon) were uniformly up-regulated along with genes for IL-10 related genes, IL-15, TH1 related chemokines, IgG Fc receptors, IL-8, IL-1beta, TGFB1, oncostatin M, ADCC signaling, complement-related genes, granzymes, and NK cell receptors. Malaria infection appeared to induce both TH17 and THalphabeta types of immunity, as neutrophil-related genes, TGFbeta1, IL-6 family gene (Oncostatin M), along with IFN-gamma and NK cytotoxicity and ADCC genes were up-regulated following infection with P. falciparum. Thus, it appears that both THabeta and TH17 types of immunity may contribute to the disease manifestations associated with and recovery from P. falciparum infection.
520 $a Conclusion. Microarray profiling revealed patterns of gene expression in PBMCs which were consistent with many of the signs and symptoms most commonly associated with acute malaria. In addition, microarray analysis provided valuable insights into how the host responds immunologically to infection with this parasite. These observations underscore the potential value of microarray profiling in delineating the pathogenesis and immunology of malaria. Gaining a better understanding of malaria immunology through this genomic approach will help develop better prevention and control strategies for malaria, including vaccines.
590 $a School code: 0098.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Parasitology. $3 1028974
650 4 $a Health Sciences, Immunology. $3 1017716
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690 $a 0718
690 $a 0982
710 2 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 68-11B.
790 $a 0098
790 1 0 $a Bourgeois, August Louis, $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288472