New insights ofHelicobacter pylorihost-pathogen interactions: The triangle of virulence factors, epigenetic modifications and non-coding RNAs

Abstract

Helicobacter pylori (H. pylori) is a model organism for understanding host-pathogen interactions and infection-mediated carcinogenesis. Gastric cancer and H. pylori colonization indicates the strong correlation. The progression and exacerbation of H. pylori infection are influenced by some factors of pathogen and host. Several virulence factors involved in the proper adherence and attenuation of immune defense to contribute the risk of emerging gastric cancer, therefore analysis of them is very important. H. pylori also modulates inflammatory and autophagy process to intensify its pathogenicity. From the host regard, different genetic factors particularly affect the development of gastric cancer. Indeed, epigenetic modifications, MicroRNA and long non-coding RNA received more attention. Generally, various factors related to pathogen and host that modulate gastric cancer development in response to H. pylori need more attention due to develop an efficacious therapeutic intervention. Therefore, this paper will present a brief overview of host-pathogen interaction especially emphases on bacterial virulence factors, interruption of host cellular signaling, the role of epigenetic modifications and non-coding RNAs.

ceRNA network construction and comparison of gastric cancer with or without Helicobacter pylori infection

“…Serum H19, LINC00152, and Lnc‐SGK1 may serve as potential biomarkers for the diagnosis of H. pylori GC (Yang et al, ; Yao et al, ). In H. pylori (+) GC serum, miR‐146, miR‐375, and Let‐7 were downregulated and miR‐19 and miR‐21 were upregulated for H. pylori clearance (Polakovicova et al, ; Vaziri, Tarashi, Fateh, & Siadat, ). miR‐124 was reported to have a protective role through the inhibition of DNA damage in the etiology of H. pylori ‐associated GC (Murray‐Stewart et al, ).…”

From Gene to Protein—How Bacterial Virulence Factors Manipulate Host Gene Expression During Infection

“…Additionally, the DNA can be methylated at cytosine or adenosine residues converting them into methyl-cytosine or methyl-adenosine to cause transcriptional repression [30]. Hypermethylation dominantly occurs at CpG islands, cytosine-guanine rich regions at promotor regions, disrupting TFs and RNA polymerase binding to DNA or recruiting other co-repressors.…”

“…Moving away from the old definition of epigenetics as hereditable stable changes at chromatin and DNA without changing its sequence, modern opinion changed towards a highly dynamic and reversible mechanism of gene regulation also enabling short term adaptions to changing environments [30]. As consequence, regulation through ncRNAs are also included to the epigenetic regulatory repertoire that can be classified according to their length into short ncRNAs (<200 nucleotides), which include miRNAs or long ncRNAs (>200 nucleotides) [33].…”

Chlamydia trachomatis induces lncRNA MIAT upregulation to regulate mitochondria‐mediated host cell apoptosis and chlamydial development

“…Studies have shown that intracellular pathogens can regulate cell signalling pathways and achieve immune escape by regulating the expression profiles of host lncRNAs, 11 such as Rickettsial , 12 Mycobacterium tuberculosis , 13 Helicobacter pylori 14 and Listeria monocytogenes . 15 C .…”

“…Studies have shown that intracellular pathogens can regulate cell signalling pathways and achieve immune escape by regulating the expression profiles of host lncRNAs, 11 such as Rickettsial, 12 Mycobacterium tuberculosis, 13 Helicobacter pylori 14 and Listeria monocytogenes. 15 C. trachomatis, as an intracellular pathogen, causes physiological changes in the host similar to those of the virus and changes the expression profile of the host mRNA, thus promoting its infection.…”