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Abstract

Background: Helicobacter pylori, a member of Epsilonproteobacteria, is a Gram-negative microaerophilic bacterium that colonizes gastric mucosa of about 50% of the human population. Although most infections caused by H. pylori are asymptomatic, the microorganism is strongly associated with serious diseases of the upper gastrointestinal tract such as chronic gastritis, peptic ulcer, duodenal ulcer, and gastric cancer, and it is classified as a group I carcinogen. The prevalence of H. pylori infections varies worldwide. prevalence among middle-aged adults is over 80 percent in many developing countries, as compared with 20 to 50 percent in industrialized countries. The infection is acquired by oral ingestion of the bacterium and is mainly transmitted within families in early childhood, Humans can also become infected with Helicobacter heilmannii, a spiral bacterium found in dogs, cats, pigs, and nonhuman primates.


Conclusion: H. pylori infection stimulates the reaction of autoantibodies with gastric epithelial cells, and this leads to gastritis. These autoantibodies can be directly induced to epithelial cells by activating complement, inducing apoptosis or provoking an antibody-dependent cytotoxic reaction resulting in subsequent tissue destruction.

Keywords

Helicobacter pylori, IgG & IgA & CD4 T Cell Responses

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Hussein Al–Mousawi, A. ., Hussein Neamah, B. alhuda ., Mohammed Chessab, R. ., Haider Aldujaili , H. ., & Mohammed Chessab, J. . (2022). Relation Helicobacter pylori with Pathogenesis of Stomach and Immune Responses . Medical Science Journal for Advance Research, 3(2), 55–60. https://doi.org/10.46966/msjar.v3i2.41
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References

  1. Roszczenko-Jasińska, P., Wojtyś, M. I., & Jagusztyn-Krynicka, E. K. (2020). Helicobacter pylori treatment in the post-antibiotics era—searching for new drug targets. Applied Microbiology and Biotechnology, 1-15.
  2. Roesler, B. M., Rabelo-Gonçalves, E. M., & Zeitune, J. M. (2014). Virulence factors of Helicobacter pylori: a review. Clinical Medicine Insights: Gastroenterology, 7, CGast-S13760
  3. Feldman RA. Epidemiologic observations and open questions about disease and infection caused by Helicobacter pylori. In: Achtman M, Suerbaum S, eds. Helicobacter pylori: molecular and cellular biology. Wymondham, United Kingdom: Horizon Scientific Press, 2001:29-51.
  4. Google Scholar. opens in new tab
  5. Rowland M, Kumar D, Daly L, O'Connor P, Vaughan D, Drumm B. Low rates of Helicobacter pylori reinfection in children. Gastroenterology 1999;117:336-341
  6. Solnick JV, Schauer DB. Emergence of diverse Helicobacter species in the pathogenesis of gastric and enterohepatic diseases. Clin Microbiol Rev 2001;14:59-97(
  7. Tomb JF, White O, Kerlavage AR, et al. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 1997;388:539-547[Erratum, Nature 1997;389:412.]
  8. Alm RA, Ling LS, Moir DT, et al. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 1999;397:176-180[Erratum, Nature 1999;397:719.]
  9. Falush D, Kraft C, Taylor NS, et al. Recombination and mutation during long-term gastric colonization by Helicobacter pylori: estimates of clock rates, recombination size, and minimal age. Proc Natl Acad Sci U S A 2001;98:15056-15061
  10. Suerbaum S, Smith JM, Bapumia K, et al. Free recombination within Helicobacter pylori. Proc Natl Acad Sci U S A 1998;95:12619-12624
  11. Bridge DR, Scott Merrell D (2013) Polymorphism in the Helicobacter pylori CagA and VacA toxins and disease. Gut Microbes 4:101–117.; McLean MH, El-Omar EM (2014) Genetics of gastric cancer. Nat Rev Gastroenterol Hepatol 11:664–674
  12. Uotani T, Miftahussurur M, Yamaoka Y (2015) Effect of bacterial and host factors on Helicobacter pylori eradication therapy. Expert Opin Ther Targets 19:1637–165
  13. Noto JM, Gaddy JA, Lee JY, Piazuelo MB, Friedman DB, Colvin DC, Romero-Gallo J, Suarez G, Loh J, Slaughter JC, Tan S, Morgan DR, Wilson KT, Bravo LE, Correa P, Cover TL, Amieva MR, Peek RM (2013) Iron deficiency accelerates Helicobacter pylori–induced carcinogenesis in rodents and humans. J Clin Invest 123:479–492
  14. Gaddy JA, Radin JN, Loh JT, Zhang F, Washington MK, Peek RM, Algood HMS, Cover TL (2013) High dietary salt intake exacerbates Helicobacter pylori- induced gastric carcinogenesis. Infect Immun 81:2258–2267
  15. Savoldi A, Carrara E, Graham DY, Conti M, Tacconelli E (2018) Prevalence of antibiotic resistance in Helicobacter pylori: a systematic review and meta-analysis in World Health Organization regions. Gastroenterology 155:1372-1382.e17
  16. Matsumoto H, Shiotani A, Graham DY (2019) Current and future treatment of Helicobacter pylori infections. Adv Exp Med Biol 1149:211–225
  17. Hill C, Guarner F, Reid G, Gibson GR, Merenstein DJ, Pot B, Morelli L, Canani RB, Flint HJ, Salminen S, Calder PC, Sanders ME (2014) Expert consensus document: the international scientific association for probiotics and prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nat Rev Gastroenterol Hepatol 11:506–514.
  18. Sarowska J, Choroszy-Król I, Regulska-Ilow B, Frej-Mądrzak M, Jama-Kmiecik A (2013) The therapeutic effect of probiotic bacteria. Adv Clin Exp Med 22:759–766
  19. Marshall BJ, Warren JR.( 1984) Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1:1311–1315.
  20. Schreiber S, Konradt M, Groll C, Scheid P, Hanauer G, Werling HO, Josenhans C, Suerbaum S. (2004)The spatial orientation of Helicobacter pylori in the gastric mucus. Proc Natl Acad Sci USA. 101:5024–5029.
  21. Semino-Mora C, Doi SQ, Marty A, Simko V, Carlstedt I, Dubois A. (2003)Intracellular and interstitial expression of Helicobacter pylori virulence genes in gastric precancerous intestinal metaplasia and adenocarcinoma. J Infect Dis. 187:1165–1177.
  22. Bauerfeind P, Garner R, Dunn BE, Mobley HL.(1997) Synthesis and activity of Helicobacter pylori urease and catalase at low pH. Gut. 1997;40:25–30.
  23. Wen Y, Feng J, Scott DR, Marcus EA, Sachs G. (2007).The HP0165-HP0166 two-component system (ArsRS) regulates acid-induced expression of HP1186 alpha-carbonic anhydrase in Helicobacter pylori by activating the pH-dependent promoter. J Bacteriol. 189:2426–2434.
  24. Eaton KA, Suerbaum S, Josenhans C, Krakowka S. (1996).Colonization of gnotobiotic piglets by Helicobacter pylori deficient in two flagellin genes. Infect Immun. 64:2445–2448.
  25. Wiedemann T, Hofbaur S, Tegtmeyer N, Huber S, Sewald N, Wessler S, Backert S, Rieder G. (2012).Helicobacter pylori CagL dependent induction of gastrin expression via a novel αvβ5-integrin-integrin linked kinase signalling complex. Gut.61:986–996.
  26. Saha A, Backert S, Hammond CE, Gooz M, Smolka AJ.(2010). Helicobacter pylori CagL activates ADAM17 to induce repression of the gastric H, K-ATPase alpha subunit. Gastroenterology. 139:239–248.
  27. Perez-Perez GI, Dworkin BM, Chodos JE, Blaser MJ. (1988).Campylobacter pylori antibodies in humans. Ann Intern Med. 109:11–17.
  28. Mattsson A, Quiding-Järbrink M, Lönroth H, Hamlet A, Ahlstedt I, Svennerholm A.(1998) . Antibody-secreting cells in the stomachs of symptomatic and asymptomatic Helicobacter pylori-infected subjects. Infect Immun. 66:2705–2712.
  29. Claeys D, Faller G, Appelmelk BJ, Negrini R, Kirchner T. (1998)The gastric H+,K+-ATPase is a major autoantigen in chronic Helicobacter pylori gastritis with body mucosa atrophy. Gastroenterology. 115:340–347.
  30. Cerutti A, Chen K, Chorny A.(2011) .Immunoglobulin responses at the mucosal interface. Annu Rev Immunol. 29:273–293.
  31. Benveniste J, Lespinats G, Salomon J. (1971).Serum and secretory IgA in axenic and holoxenic mice. J Immunol. 107:1656–1662.
  32. Benveniste J, Lespinats G, Adam C, Salomon JC.(1971). Immunoglobulins in intact, immunized, and contaminated axenic mice: study of serum IgA. J Immunol. 107:1647–1655.
  33. Kaneko T, Ota H, Hayama M, Akamatsu T, Katsuyama T.(2000). Helicobacter pylori infection produces expression of a secretory component in gastric mucous cells. Virchows Arch. 437:514–520.
  34. Ahlstedt I, Lindholm C, Lönroth H, Hamlet A, Svennerholm AM, Quiding-Järbrink M. (1999) .Role of local cytokines in increased gastric expression of the secretory component in Helicobacter pylori infection. Infect Immun. 67:4921–4925.
  35. Meyer F, Wilson KT, James SP. (2000).Modulation of innate cytokine responses by products of Helicobacter pylori. Infect Immun. 68:6265–6272.
  36. Quiding-Järbrink M, Sundström P, Lundgren A, Hansson M, Bäckström M, Johansson C, Enarsson K, Hermansson M, Johnsson E, Svennerholm AM.(2009). Decreased IgA antibody production in the stomach of gastric adenocarcinoma patients. Clin Immunol. 131:463–471 .
  37. Birkholz S, Schneider T, Knipp U, Stallmach A, Zeitz M. (1998). Decreased Helicobacter pylori-specific gastric secretory IgA antibodies in infected patients. Digestion. 59:638–645.
  38. Nurgalieva ZZ, Conner ME, Opekun AR, Zheng CQ, (2005).Elliott SN, Ernst PB, Osato M, Estes MK, Graham DY. B-cell and T-cell immune responses to experimental Helicobacter pylori infection in humans. Infect Immun. 73:2999–3006.
  39. Feng T, Elson CO. (2011). Adaptive immunity in the host-microbiota dialog. Mucosal Immunol. 4:15–21.
  40. Konrad A, Cong Y, Duck W, Borlaza R, Elson CO.(2006) Tight mucosal compartmentation of the murine immune response to antigens of the enteric microbiota. Gastroenterology. 2006;130:2050–2059

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