Journals / Mikrobiyoloji Bülteni / 2008 / Cilt: 42 - Sayı: 1

Helicobacter pylori infection and phagocytosis

Helicobacter pylori enfeksiyonu ve fagositoz

Pages
177–184
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this review article, the correlation between H.pylori infection and innate immune response with emphasis on the avoidance of killing by phagocytosis, have been discussed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Helicobacter pylori is a chronic infectious agent defined as the major pathogen causing gastritis, gastric and duodenal ulcer, gastric carcinoma and mucosa associated lenfoid tissue (MALT) lymphoma.
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Key Findings & Data:H.pylori is the only microorganism known to get colonized in human stomach and inhabit in gastric mucosal cells.
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Conclusion & Impact:In this review article, the correlation between H.pylori infection and innate immune response with emphasis on the avoidance of killing by phagocytosis, have been discussed.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Helicobacter pylori is a chronic infectious agent defined as the major pathogen causing gastritis, gastric and duodenal ulcer, gastric carcinoma and mucosa associated lenfoid tissue (MALT) lymphoma. H.pylori is the only microorganism known to get colonized in human stomach and inhabit in gastric mucosal cells. To achieve this, H.pylori must escape from both innate and adaptive immune responses. The host immune response is unable to eliminate the infection and this is generally associated with pathogenesis. The persistence of the induced H.pylori infection suggests that the response is not effective to eliminate the infection. In this review article, the correlation between H.pylori infection and innate immune response with emphasis on the avoidance of killing by phagocytosis, have been discussed.

Özet

Helicobacter pylori gastrit, gastrik ve duodenal ülserler, gastrik karsinoma ve mukoza ile ilişkili lenfoid doku (MALT) lenfomasında temel patojen olarak tanımlanmış kronik enfeksiyon etkeni olan bir bakteridir. H.pylori midede kolonize olabilen tek mikroorganizmadır ve gastrik mukus salgılayan hücrelerde yerleşme özelliğine sahiptir. Bunun için hem doğal hem de kazanılmış bağışık yanıt mekanizmalarından kaçması gerekmektedir. Konağın bağışık yanıtı, enfeksiyonu yok edememekte ve ilginç olarak da patogenezle ilişkilendirilmektedir. Enfeksiyon varlığında oluşan yanıtın enfeksiyonu yok etmede etkili olmadığı düşünülmektedir. Bu derleme yazıda, H.pylori enfeksiyonu ve doğal bağışık yanıt arasındaki ilişki ile bakterinin fagositozdan kaçış mekanizmaları tartışılmıştır.

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Cite This Article

GÜRBÜZ, E. D., BEKMEN, N. (2008). Helicobacter pylori infection and phagocytosis. Mikrobiyoloji Bülteni, Cilt: 42 - Sayı: 1, 177–184. https://ajindex.com/articles/298989

References (15)

  1. Allen LA. The role of the neutrophil and phagocytosis in infection caused by Helicobacter pylori. Curr Opin Infect Dis 2001; 14: 273-7
  2. Beswick EJ, Suarez G, Reyes VE. H.pylori and host interactions that influence pathogenesis. World J Gastroenterol 2006; 12: 5599-605
  3. Algood HM, Cover TL. Helicobacter pylori persistence: an overview of interactions between H.pylori and host immun defenses. Clin Microbiol Rev 2006; 19: 597-613
  4. Bergman M, Del Prete G, van Kooyk Y, Appelmelk B. Helicobacter pylori phase variation, immune modulation and gastric autoimmunity. Nature 2006; 4: 151-9
  5. Chmiela M, Czkwianianc E, Wadstrom T, Rudnicka W. Role of Helicobacter pylori surface structures in bacterial interaction with macrophages. Gut 1997; 40: 20-4
  6. Ferrero RL. Innate immune recognition of the extracellular mucosal pathogen, Helicobacter pylori. Mol Immunol 2005; 42: 879-85
  7. Allen LA. Phagocytosis and persistence of Helicobacter pylori. Cell Microbiol 2007; 9: 817-28
  8. Odenbreit S, Gebert B, Puis J, et al. Interaction of Helicobacter pylori with professional phagocytes: role of the cag pathogenicity island and translocation, phosphorylation and processing of CagA. Cell Microbiol 2001; 3: 21-31
  9. Allen LA, Schlesinger LS, Kang B. Virulent strains of Helicobacter pylori demonstrate delayed phagocytosis and stimulate homotypic phagosome fusion in macrophages. J Exp Med 2000; 191:115-27
  10. Luzza F, Parrello T, Monteleone G, et al. Up-regulation of IL-17 is associated with bioactive IL-8 expression in Helicobacter pylori-Infected human gastric mucosa. J Immunol 2000; 165: 5332-7
  11. Mandell L, Moran AP, Cocchiarella A, Houghton JM. Intact Gram negative Helicobacter pylori, Helicobacter felis, and Helicobacter hepaticus bacteria activate innate immunity via Toll-Like Receptor 2 but not Toll-Like Receptor 4. Infect Immun 2004; 72: 6446-54
  12. Abbas AK, Lichtman AH. Cellular and Molecular Immunology, pp: 275-97. 2003, 5th ed. Elsevier Science, USA
  13. Unemo M, Aspholm-Hurtig M, liver D, et al. The sialic acid binding SabA adhesin of Helicobacter pylori is essential for nonopsonic activation of human neutrophils. J Biol Chem 2005; 280: 15390-7
  14. Satin B, Giudice GD, Bianca VD, et al. The neutrophil-activating protein (HP-NAP) of Helicobacter pylori is a protective antigen and a major virulence factor. J Exp Med 2000; 191: 1467-76
  15. Ramarao N, Gray-Owen SD, Backed S, Meyer TF. Helicobacter pylori inhibits phagocytosis by professional phagocytes