Unknown,Transcriptomics,Genomics,Proteomics

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Comparative Analysis of Gene Expression Profiles in Infective and Developing Larvae of Brugia malayi and Brugia pahangi

ABSTRACT: Comparative analysis of gene expression profiles provided novel insights into the genes that are transcriptionally active in infective and developing larvae of two closely related species. Species differences may indicate different metabolic adaptations that could affect host specificity, tissue tropism, and pathogenicity Two biological replicates of infective (L3) or developing larval RNA used for hybridization, in duplicate, to examine the gene expression changes in Brugia larvae Brugia malayi vector derived third stage larvae (Bm VL3); Brugia pahangi vector derived third stage larvae (Bp VL3); Brugia pahangi L3 cultured in vitro (Bp cL3); Brugia pahangi L3 derived from peritoneal cavity of infected gerbils (Bp ipL3); Brugia pahangi migrating L3 (Bp mL3) from infected gerbils

ORGANISM(S): Brugia malayi

SUBMITTER: Michael Heinz

PROVIDER: E-GEOD-68301 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Filarial nematodes are arthropod-borne nematodes that cause a variety of economically important diseases such as onchocerciasis (river blindness), lymphatic filariasis, and heartworm disease. The most widespread filarial disease of humans is lymphatic filariasis, caused by worms in the genera Wuchereria and Brugia. Lymphatic filariasis is an economic and social burden in endemic countries and affects approximately 119 million people worldwide (Michael, 1997). In humans, the worms live in and block the lymph vessels, causing improper flow of lymph, and inflammation of the lymphatic system. The symptoms are fever, swollen limbs and genitals, generalized malaise, and can progress to a debilitating condition known as elephantiasis This research focuses on the transmission of these worms to the disseminating mosquito host, and it is based on the interesting observation that mf must be at least 7 days old to successfully infect the mosquito (de Hollanda, 1982). Newborn mf that have not â??maturedâ?? cannot successfully penetrate the midgut of the mosquito, and subsequently cannot develop to the L3 stage (Fuhrman, 1987). Previous work done by another group 20 years ago suggests that the molecular makeup of the worm surface changes during this maturation process (Furman, 1983 a and b). We used microarray analysis to characterize changes in gene expression that take place during the mf maturation process. Understanding the gene expression changes that occur as the mf mature will allow us to understand the nature of the philological transition that allows mf to move from the human to the mosquito host. With this information in hand, we can eventually identify parasite molecules that could be targeted to either stop parasite reproduction or prevent transmission of the mf to the mosquito. This would stop parasite transmission in endemic areas. This SuperSeries is composed of the following subset Series: GSE14939: Brugia pahangi mature vs immature microfilariae GSE14940: Brugia malayi mature vs immature microfilariae Refer to individual Series

Project description:Filarial nematodes are arthropod-borne nematodes that cause a variety of economically important diseases such as onchocerciasis (river blindness), lymphatic filariasis, and heartworm disease. The most widespread filarial disease of humans is lymphatic filariasis, caused by worms in the genera Wuchereria and Brugia. Lymphatic filariasis is an economic and social burden in endemic countries and affects approximately 119 million people worldwide (Michael, 1997). In humans, the worms live in and block the lymph vessels, causing improper flow of lymph, and inflammation of the lymphatic system. The symptoms are fever, swollen limbs and genitals, generalized malaise, and can progress to a debilitating condition known as elephantiasis This research focuses on the transmission of these worms to the disseminating mosquito host, and it is based on the interesting observation that mf must be at least 7 days old to successfully infect the mosquito (de Hollanda, 1982). Newborn mf that have not â??maturedâ?? cannot successfully penetrate the midgut of the mosquito, and subsequently cannot develop to the L3 stage (Fuhrman, 1987). Previous work done by another group 20 years ago suggests that the molecular makeup of the worm surface changes during this maturation process (Furman, 1983 a and b). We used microarray analysis to characterize changes in gene expression that take place during the mf maturation process. Understanding the gene expression changes that occur as the mf mature will allow us to understand the nature of the philological transition that allows mf to move from the human to the mosquito host. With this information in hand, we can eventually identify parasite molecules that could be targeted to either stop parasite reproduction or prevent transmission of the mf to the mosquito. This would stop parasite transmission in endemic areas. Brugia pahangi mature mf (30 days and older) RNA was compared to immature mf (3 days and younger). Three biological replicates were performed each with two technical replicates

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Comparative Analysis of Gene Expression Profiles in Infective and Developing Larvae of Brugia malayi and Brugia pahangi

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