ArticleScientific reports2015
Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
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- Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling.Journal of immunology research · 2022Article
- An Overview ofMicroorganisms · 2021Review
- Podoplanin Drives Motility of Active MacrophageFrontiers in immunology · 2021Article
- Infection withPathogens (Basel, Switzerland) · 2020Article
- Article
- Construction of an integrated gene regulatory network link to stress-related immune system in cattle.Genetica · 2017Article
- Nuclear carbonic anhydrase 6B associates with PRMT5 to epigenetically promote IL-12 expression in innate response.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mycobacterium tuberculosis arrests host cycle at the G1/S transition to establish long term infection.PLoS pathogens · 2017Article
- Regulation of Epigenetic Modifiers, Including KDM6B, by Interferon-γ and Interleukin-4 in Human Macrophages.Frontiers in immunology · 2017Article
- Helicobacter pylori Eradication Causes Perturbation of the Human Gut Microbiome in Young Adults.PloS one · 2016Article
- Genome-Wide Transcription Study of Cryptococcus neoformans H99 Clinical Strain versus Environmental Strains.PloS one · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori at multiplicity of infection (MOI ≥ 50) have been shown to cause apoptosis in RAW264.7 monocytic macrophage cells. Because chronic gastric infection by H. pylori results in the persistence of macrophages in the host's gut, it is likely that H. pylori is present at low to moderate, rather than high numbers in the infected host. At present, the effect of low-MOI H. pylori infection on macrophage has not been fully elucidated. In this study, we investigated the genome-wide transcriptional regulation of H. pylori-infected RAW264.7 cells at MOI 1, 5 and 10 in the absence of cellular apoptosis. Microarray data revealed up- and down-regulation of 1341 and 1591 genes, respectively. The expression of genes encoding for DNA replication and cell cycle-associated molecules, including Aurora-B kinase (AurkB) were down-regulated. Immunoblot analysis verified the decreased expression of AurkB and downstream phosphorylation of Cdk1 caused by H. pylori infection. Consistently, we observed that H. pylori infection inhibited cell proliferation and progression through the G1/S and G2/M checkpoints. In summary, we suggest that H. pylori disrupts expression of cell cycle-associated genes, thereby impeding proliferation of RAW264.7 cells, and such disruption may be an immunoevasive strategy utilized by H. pylori.
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