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Gene expression profiling in mouse liver infected with Clonorchis sinensis metacercariae
Authors:Dong Min Kim  Byung-Sam Ko  Jung-Won Ju  Shin-Hyeong Cho  Suk-Jin Yang  Young Il Yeom  Tong-Soo Kim  Yonggwan Won  Il-Chul Kim
Affiliation:1. BK21 Ubiquitous Information Appliances, Chonnam National University, Gwangju, Republic of Korea
2. Department of Biological Sciences, Chonnam National University, 300 Yongbongdong, Buk-gu, Gwangju, 500-757, Republic of Korea
3. Division of Malaria and Parasitic Diseases, National Institute of Health, Seoul, 122-701, Republic of Korea
4. Medical Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, P.O. Box?115, Daejeon, 305-806, Republic of Korea
5. Department of Parasitology, College of Medicine, Inha University, Incheon, 400-712, Republic of Korea
Abstract:
Clonorchis sinensis, the parasite that causes clonorchiasis, is endemic in many Asian countries, and infection with the organism drives changes in the liver tissues of the host. However, information regarding the molecular events in clonorchiasis remains limited, and little is currently known about host–pathogen interactions in clonorchiasis. In this study, we assessed the gene expression profiles in mice livers via DNA microarray analysis 1, 2, 4, and 6 weeks after induced metacercariae infection. Functional clustering of the gene expression profile showed that the immunity-involved genes were induced in the livers of the mice at the early stage of metacercariae infection, whereas immune responses were reduced in the 6-week liver tissues after infection in which the metacercariae became adult flukes. Many genes involved in fatty acid metabolism, including Peci, Cyp4a10, Acat1, Ehhadh, Gcdh, and Cyp2 family were downregulated in the infected livers. On the other hand, the liver tissues infected with the parasite expressed Wnt signaling molecules such as Wnt7b, Fzd6, and Pdgfrb and cell cycle-regulating genes including cyclin-D1, Cdca3, and Bcl3. These investigations constitute an excellent starting point for increased understanding of the molecular mechanisms underlying host–pathogen interaction during the development of C. sinensis in the host liver.
Keywords:
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