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  • Helicobacter pylori-induced inflammation's role in the development of an epigenetic field defect and its applicability as a measure of exposure and cancer risk.

  • Pouria Khodaei Ataloo,1,*
    1. Department of Microbiology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran


  • Introduction: Several investigations have demonstrated that some infectious pathogens may cause epigenetic modifications, such as host gene methylation, which can trigger the development and spread of several illnesses, most notably cancer. The inherited epigenetic modifications in host transcription that enable persistent infection-causing microbes to stay latent or chronic without requiring constant expression of proteins that originate and sustain a particular habitat are probably advantageous. A Helicobacter pylori (H. pylori) infection in the human stomach mucosa is the most extensively researched chronic bacterial infection linked to cancer. As of right now, a lot of bacterial-induced chromatin changes, like histone acetylation/deacetylation and phosphorylation/dephosphorylation, happen when bacterial components (like metabolites, virulence factors, and microbial-associated molecular patterns) trigger the host cell signaling cascade. H. pylori, a carcinogenic bacterium, may also alter histones through a variety of methods, such as by altering the mitogen-activated protein kinase (MAPK) pathway. The majority of known bacterial epigenetic systems control certain DNA-protein interactions by using DNA methylation as a signal. There is a growing understanding of the connection between bacterial infections and DNA methylation. The most notable example is H. pylori infection, which greatly affects the promoters of methylated genes in gastric cancer cells and results in abnormal DNA methylation in the human stomach mucosa. H. pylori-related hypermethylation can be seen, for instance, in the CpG islands of miRNA genes, the E-cadherin gene in CDH1, tumor suppressor genes, and DNA repair genes. Additionally, H. pylori-mediated inflammation results in the release of lymphocytes and the infiltration of macrophages, which seem to be crucial in triggering methylation in response to ethanol or NaCl stimuli, which stimulate neutrophil infiltration into the stomach (Figure 3). One important acquired risk factor for stomach cancer is H. pylori. Numerous proteins and antigens (CagA, FlaA, and VacA) present in this bacterium contribute significantly to its pathogenicity. Furthermore, it has been shown that H. pylori indirectly affects DNA integrity and cell proliferation by aberrant DNA methylation, which is a key factor in the development of gastric cancer. This is compelling evidence that a bacterial infection may cause epigenetic modifications in a tissue, which might result in long-lasting alterations in gene expression.
  • Methods: The PubMed, Scopus, and Google Scholar databases were searched for papers for this review research. The most significant recent studies on how bacteria can change epigenetic markers and cause or contribute to the development of different illnesses are covered in this article.
  • Results: Evidence of how bacterial infections alter host cell epigenetic information in a variety of ways is mounting. Thanks to recent technical developments, it is now feasible to profile histone modifications and map the DNA methylation throughout the human genome. These new technologies will surely help bacteria that are responsible for chromatin modifications in mammalian cells. Transcription, cell division, DNA repair, and replication are all regulated by epigenetics.
  • Conclusion: Eukaryotic complex genomes require greater levels of control, including DNA modifications, post-translational histone modifications, and chromatin remodeling, in addition to sequence-specific DNA-binding factors. A common term for these modifications is "epigenetic." The pathophysiology of chronic illnesses is significantly influenced by microorganisms' capacity to epigenetically alter host gene expression. Infectious bacterial infections may be linked to the loss of epigenetic control over these DNA-based mechanisms. Improved knowledge of the relationship between the epigenome and bacterial infectious illnesses creates therapeutic prospects, especially for the reversal of epigenetic changes and the creation of more potent medicinal molecules. Furthermore, the prompt elimination of pathogen-induced patho-epigenetic alterations may avert autoimmune disorders, some types of cancer, and latent or chronic infections.
  • Keywords: epigenetic, Helicobacter pylori, stomach cancer

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