Gene expression profiling of human promyelocytic cells in response to infection with Anaplasma phagocytophilum

被引:61
作者
de la Fuente, J [1 ]
Ayoubi, P
Blouin, EF
Almazán, C
Naranjo, V
Kocan, KM
机构
[1] Oklahoma State Univ, Ctr Vet Hlth Sci, Dept Vet Pathobiol, Stillwater, OK 74078 USA
[2] UCLM, CSIC, JCCM, Inst Invest Recursos Cineget IREC, Ciudad Real 13005, Spain
[3] Oklahoma State Univ, Dept Biochem & Mol Biol, Micoarray Core Facil, Stillwater, OK 74078 USA
关键词
D O I
10.1111/j.1462-5822.2004.00485.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Anaplasma phagocytophilum (Rickettsiales: Anaplasmataceae) causes human, equine and canine granulocytic anaplasmosis and tick-borne fever of ruminants. The rickettsia parasitizes granulocytes and bone marrow progenitor cells, and can be propagated in human promyelocytic and tick cell lines. In this study, microarrays of synthetic polynucleotides of 21 329 human genes were used to identify genes that are differentially expressed in HL-60 human promyelocytic cells in response to infection with A. phagocytophilum. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) of selected genes confirmed the results of the microarray analysis. Six genes in the A. phagocytophilum-infected cells were found to be upregulated greater than 30-fold, while expression of downregulated genes most often did not change more than sixfold. Genes that were found to be differentially regulated in infected cells were those essential for cellular mechanisms including growth and differentiation, cell transport, signalling and communication and protective response against infection, some of which are most likely necessary for infection and multiplication of A. phagocytophilum in host cells. The differentially regulated genes described herein provide new information on the gene expression profiles in A. phagocytophilum-infected HL-60 cells, thus expanding in a global manner the existing information on the response of mammalian cells to A. phagocytophilum infection.
引用
收藏
页码:549 / 559
页数:11
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