作者: Jamuna Vadivelu , Mun Fai Loke , Won Fen Wong , Grace Min Yi Tan , Chung Yeng Looi
DOI: 10.1038/SREP11046
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摘要: Helicobacter pylori at multiplicity of infection (MOI ≥ 50) have been shown to cause apoptosis in RAW264.7 monocytic macrophage cells. Because chronic gastric by H. results the persistence macrophages host's gut, it is likely that present low moderate, rather than high numbers infected host. At present, effect low-MOI on has not fully elucidated. In this study, we investigated genome-wide transcriptional regulation pylori-infected cells MOI 1, 5 and 10 absence cellular apoptosis. Microarray data revealed up- down-regulation 1341 1591 genes, respectively. The expression genes encoding for DNA replication cell cycle-associated molecules, including Aurora-B kinase (AurkB) were down-regulated. Immunoblot analysis verified decreased AurkB downstream phosphorylation Cdk1 caused infection. Consistently, observed inhibited proliferation progression through G1/S G2/M checkpoints. summary, suggest disrupts thereby impeding cells, such disruption may be an immunoevasive strategy utilized pylori.