<i>Helicobacter</i><i>pylori</i>-induced modification of the histone H3 phosphorylation status in gastric epithelial cells reflects its impact on cell cycle regulation

Fehri, Lina Fassi; Rechner, Cindy; Janßen, Sabrina; Mak, Tim N.; Holland, Carsten; Bartfeld, Sina; Brüggemann, Holger; Meyer, Thomas

doi:10.4161/epi.4.8.10217

Cited by 60 publications

(37 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, Trp53 can direct E2f2-mediated growth arrest involving the target gene Gadd45. 40 E2f2 and Gadd45 are two genes that were upregulated in the Salmonella-susceptible B6.MOLF-Ity/ Ity2.RecD congenic strain, which further supports the [41][42][43] We showed here that Trp53 expression is affected by specific Ity2A genomic context, and we speculate that its impact on resistance to Salmonella infection is explained by favoring a cell-cycle arrest state allowing the bacteria to proliferate more successfully. Therefore, we conclude that the MOLF/Ei allele at Ity2 maintains the levels of Trp53 expression within a range that allows control of bacterial growth during infection, a situation that is beneficial to the host.…”

Section: Discussionsupporting

confidence: 78%

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

et al. 2011

View full text Add to dashboard Cite

Typhoid fever, which is caused by Salmonella typhi and paratyphi, is a severe systemic disease that remains a major public health issue in several areas of the world. We can model the human disease using mice infected with a related bacterium, Salmonella typhimurium. This model recapitulates several clinical aspects of the human disease and allows for the study of the host response to Salmonella typhimurium infection in vivo. Previous work in our laboratory has identified three Immunity to typhimurium loci (Ity, Ity2 and Ity3) in the wild-derived MOLF/Ei mice, influencing survival after infection with Salmonella typhimurium. The MOLF/Ei alleles at Ity and Ity2 are protective, while the MOLF/Ei allele at Ity3 confers susceptibility. In this paper, we have generated a novel cross combination between the highly susceptible strain, MOLF/Ei, and the resistant strain, 129S6, to better define the genetic architecture of susceptibility to infection in MOLF/Ei. Using this cross, we have replicated the locus on chr 11 (Ity2) and identified a novel locus on chr 13 (Ity13). Using microarrays and transcriptional profiling, we examined the response of uninfected and infected Ity2 congenic mice. These analyses demonstrate a role for both type-1-interferon (IFN) and TRP53 signaling in the pathogenesis of Salmonella infection.

show abstract

Section: Discussionsupporting

confidence: 78%

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

et al. 2011

View full text Add to dashboard Cite

show abstract

“…3) (Pathak et al 2006). In contrast, in gastric epithelial cells H. pylori has an opposite effect by inducing dephosphorylation of H3S10 and H3T3, as well as deacetylation of H3K23 (Fehri et al 2009;Ding et al 2010a). H. pylorimediated chromatin modifications are in this case dependent on a functional type IV secretion system, suggesting involvement of an injected bacterial product.…”

Section: Bacterial Targeting Of Chromatinmentioning

confidence: 99%

“…H. pylorimediated chromatin modifications are in this case dependent on a functional type IV secretion system, suggesting involvement of an injected bacterial product. H. pylori-induced dephosphorylation of H3S10 is transient and impacts both the cell cycle (Fehri et al 2009) and transcription of oncogene c-Jun ( positively) and heat shock gene hsp70 (negatively) (Ding et al 2010a). H. pylori-mediated premitotic arrest involves dephosphorylation of H3S10 upon deregulation of the mitotic histone kinase VRK1, followed by rephosphorylation of H3S10 by an IKKa-dependent pathway.…”

Section: Bacterial Targeting Of Chromatinmentioning

confidence: 99%

Epigenetics and Bacterial Infections

Bierne¹,

Hamon²,

Cossart³

2012

Cold Spring Harbor Perspectives in Medicine

303

218

View full text Add to dashboard Cite

Epigenetic mechanisms regulate expression of the genome to generate various cell types during development or orchestrate cellular responses to external stimuli. Recent studies highlight that bacteria can affect the chromatin structure and transcriptional program of host cells by influencing diverse epigenetic factors (i.e., histone modifications, DNA methylation, chromatin-associated complexes, noncoding RNAs, and RNA splicing factors). In this article, we first review the molecular bases of the epigenetic language and then describe the current state of research regarding how bacteria can alter epigenetic marks and machineries. Bacterial-induced epigenetic deregulations may affect host cell function either to promote host defense or to allow pathogen persistence. Thus, pathogenic bacteria can be considered as potential epimutagens able to reshape the epigenome. Their effects might generate specific, long-lasting imprints on host cells, leading to a memory of infection that influences immunity and might be at the origin of unexplained diseases.

show abstract

“…There are reports that show host cell signalling mediates changes in the epigenetic modifications at specific gene loci in response to bacterial infection 12,13 . Other reports have provided proof of epigenetic modification by a bacterial protein.…”

mentioning

confidence: 99%

Mycobacteria modulate host epigenetic machinery by Rv1988 methylation of a non-tail arginine of histone H3

et al. 2015

View full text Add to dashboard Cite

Helicobacterpylori-induced modification of the histone H3 phosphorylation status in gastric epithelial cells reflects its impact on cell cycle regulation

Cited by 60 publications

References 35 publications

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

Epigenetics and Bacterial Infections

Mycobacteria modulate host epigenetic machinery by Rv1988 methylation of a non-tail arginine of histone H3

Contact Info

Product

Resources

About