In this review, we mainly focus on the persistent colonization of Helicobacter pylori in the human intestine. In recent times we have discovered new strategies used by this bacteria which may be the cause of a prolonged existence in humans or an evolution with another bacteria to optimize its existence. The balance between the bacteria and human cells in response played an important role in the persistence of the bacteria in its colonization or confers a risk of organ dysfunction leading to more serious diseases such as gastric adenocarcinoma, lymphoma, gastric peptic ulcers and many others. . A recently discovered novel factor is the secreted protease HtrA (high temperature requirement A), which has been shown to cleave the ectodomain of E-cadherin, an important cell adhesion protein and tumor suppressor, having crucial consequences on the disruption of the epithelial barrier. functions Some of the factors essential for the survival of Helicobacter pylori bacteria in the human gut and leading to a number of serious diseases are: Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay 1) Urease: The pH of the human stomach is known to be around 2.5. Since Helicobacter pylori is not acidophilic, it is not possible for it to survive in such a hostile environment (.Eaton KA, Brooks CL, Morgan DR, Krakowka S. Essential role of urease in the pathogenesis of gastritis induced by Helicobacter pylori in gnotobiotic piglets Infect Immun 1991; which ultimately increases the pH of the stomach and allows the bacteria to survive. in such a low pH in the periplasm, thereby contributing to the proton motive force (. Stingl K, Altendorf K, Bakker EP. Acidic survival of Helicobacter pylori: how urease activity triggers homeostasis of cytoplasmic pH? Trends Microbiol 2002; 10: 70-74 [PMID: 11827807 DOI: 10.1016/S0966-842X(01)02287-9]) Another mechanism by which urease leads to a periplasmic buffer may be the conversion of CO2 into bicarbonate by the action of periplasmic alpha carbonic anhydrase. (Marcus EA, Moshfegh AP, Sachs G, Scott DR. Periplasmic alpha-carbonic anhydrase activity of Helicobacter pylori is essential for acid acclimation. J Bacteriol 2005; 187: 729-738 [PMID: 15629943 DOI: 10.1128/JB.187.2. 729-738.2005]).The presence of urease provides strong evidence for persistent Helicobacter pylori colonization in humans and may perhaps serve as evidence that Helicobacter pylori persistence does not. is found in no part of the human body since the body's normal pH. is greater than 7. Therefore, further alkalization of the environmental pH can inhibit the growth of Helicobacter pylori. (Factors involved in the colonization of the human stomach by Helicobacter pylori2) Helical shape of Helicobacter pylori: Although this does not seem to be an inessential factor, it plays an important role in the pathological process of the bacteria during invasion of the stomach lining. bacteria in the human intestine. It provides a mechanistic screw-like movement that facilitates penetration into the epithelium. Apparently, the genes responsible for the morphology of the bacteria are Ccrp89, Ccrp58, Ccrp1142 and Ccrp1143. any deletion or mutation may be directly responsible for its colonization. (Bansal R, Celli JP, Hardcastle JM, Turner BS. The Influence of Mucus Microstructure andRheology in Helicobacter pylori Infection. Front Immunol 2013; 4: 310 [PMID: 24133493 DOI: 10.3389/fimmu.2013.00310])3) Mediated by Cag A strategy persists in Helicobacter pylori:Cag A bacterial protein has a site that interacts with several host kinases at the phosphorylation site. The phosphorylation site consists of an amino acid sequence called EPIGYA.M. Stein, F. Bagnoli, R. Halenbeck, R. Rappuoli, WJ Fantl, A. Covacci, c-Src/Lyn kinases activate Helicobacter pylori CagA by tyrosine phosphorylation of EPIYA motifs, Mol. Microbiol. 43 (2002) 971e980 Role of Src kinases and all kinases in the persistence of Cag A protein in H.pylori: CagA is phosphorylated by Src kinases and can then interfere with intracellular signaling pathways, leading to cell proliferation , cytoskeletal rearrangement, cell proliferation. loss of cell adhesion, remodeling of the extracellular matrix and activation of the β-catenin pathway. Based on the geographical modification of the amino acid sequence present in the Cag A gene, the variability of the pathogenicity of the gene present in the bacteria is determined. Cag A has many other effects on epithelial cells when bound, which can disrupt cell polarity and affect several host cell pathways. (Amieva MR, El-Omar EM. 2008. Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology 134:306–323) Cag PAI (Cag pathogenicity island) is a locus on DNA found that contains approximately 30 gene groups; encode the gene responsible for cagA for glutamate racemase, which would be at the origin of horizontal gene transfer. The pathogenicity of the bacteria strongly depends on the inflammatory response of the host cell which depends on the presence or absence of the pathogenicity island on the DNA locus and the severity of its evolution. For example, cag+ may be associated with a higher ratio of peptic ulcer to gastric ulcer than in the individual with negative or intermediate strains of Helicobacter pylori infections. 4) T4SS type 4 secretion system: Cag A protein is secreted via the type IV secretion system (T4SS) in gastric epithelial cells, where it plays a central role in the etiology of Helicobacter pylori-associated gastric cancer. There are essentially 15 genes on the pathogenicity island required for induction of T4SS, IL-8 and Cag A translocation or nucleotide-binding oligomerization domain (NOD1) signaling key host-pathogen interactions for conception new interventions against Helicobacter pylori. It is a contact-dependent multi-subunit secretion system that is encoded by the Cag pathogenicity island and transferred to the host cell. The association between T4SS and Cag A is strongly linked to the severity of immunological responses which can often lead to gastric adenocarcinoma and peptic ulcer disease. (Life in the Human Stomach: Persistence Strategies of the Bacterial Pathogen Helicobacter pylori.)5) VacA Toxin: Another secretory protein alongside Cag A is Vac A. VacA is a pore-forming toxin that impairs cellular function and impairs cell function. mitochondria, it permeates the plasma membrane. The Vac A genes are present in every strain of Helicobacter pylori, but also cause each strain to have a different extent of the disease process. ). Front Cell Infect Microbiol. 2012; 2:37. [PubMed: 22919629] ) localized pathogenic genes can cause programmed cell death or act as immunosuppressants, meaning they can inhibit the development of T lymphocytes. Helicobacter pylori has major antigenic determinants which are VacA and GGT (? -glutamyltranspeptidase). These two factors are involved in the maturation of dendritic cells and suppress the activity of Tregs (regulation of T lymphocytes), thus developing tolerance against T lymphocytes. Oertli M, Noben M, Engler DB et al. Helicobacter pylori gamma-glutamyl transpeptidase and vacuolating cytotoxin promote gastric persistence and immune tolerance. Proc Natl Acad Sci US A. 2013; 110:3047-52. [PubMed:23382221] This helps Helicobacter pylori, an exceptional quality, to resist innate and adaptive immunity by escaping Th1/Th17 cells - effector cells polarized to adaptation and the influence of the host system. Müller A, OertliM, Arnold IC (2011) H. pylori exploits and manipulates innate and adaptive immune cell signaling pathways to establish persistent infection. CellCommun Signal 9(1):25.6) Motility: Possession of flagella was found to be a key factor in colonization and persistence in the human gut. The presence of flagellar appendages helps the bacteria in motility and confers endurance. Evidence from the mutant bacteria lacking flagella affected its motility as well as its aftereffects in its host. The flagella push it into the mucous membranes of the host's epithelium, which allows it to survive even more easily in such an atmosphere since Helicobacter pylori is not an acidophile, it leads it to a more hospitable environment, it i.e. towards the mucous membrane of the gastric epithelium and the abundance of ammonium carbonate and neutral pH. , amino acids and cholesterol via chemotactic properties (beyond the stomach). For complete motility in the bacteria, the expression of two proteins is very crucial, namely Fla A and FlaB regulated by Flh A. Any mutant absent in this protein can lead to variability in movements, infection and therefore the persistence. Flagella function has been found to be regulated by quorum sensing using pheromones such as autoinducer-2 when responding in the environment (.Rader BA, Campagna SR, Semmelhack MF, Bassler BL, Guillemin K. The quorum sensing molecule autoinducer2 regulates motility and flagellar morphogenesis in Helicobacter pylori 2007; 189: 6109-6117 [PMID: 17586631 DOI: 10.1128/JB.00246-07]45) (Shen F , Hobley L, Doherty N, Loh JT, Cover TL, Sockett RE, Hardie KR, Atherton JC, autoinducer-2, but not LuxS/McCabe-catalyzed reverse transsulfuration, regulates motility through modulation. of flagellar gene transcription 2010:210 ;? of infection (Asakura H, Churin Y, Bauer B, Boettcher JP, Bar-. *tfeld S, Hashii N, Kawasaki N, Mollenkopf HJ, Jungblut PR, Brinkmann V, Meyer TF. Helicobacter pylori HP0518 affects flagellin glycosylation to alter bacterial motility. Mol Microbiol2010; 78:1130-1144 [PMID: 21091500 DOI: 10.1111/j.1365-2958.2010.07393.x])7) TNF-a All strains of Helicobacter pylori are believed to contain TNF-a factor encoded by the Tipa gene which as well as various chemokines such as NF-βB. for new genes involved in the induction of TNF-a gene expression in gastric epithelial cells and identified a new gene encoding a TNF-a inducing protein, which we named IPA. (M. Suganuma, M. Kurusu, K. Suzuki, et al., Novel tumor necrosis factor-inducing protein released by Helicobacter pylori for gastric cancer progression, J. Cancer Res. Clin. Oncol. 131 (2005) 305 -313. )TNF-a Tip inducer gene which, upon invasion into the host body, induces, 73: 803–811.)