Immunological aspects of Helicobacter pylori infection

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Host defence against Helicobacter pylori infection is a complex system of both specific and non-specific reactions. Among the non-specific defense mechanisms acting on bacteria before they reach the mucus layer in the stomach are digestive enzymes, lyzozyme, lactoferrin and other components with antimicrobal activity. The mucus layer is the final non-specific barrier against the bacteria reaching the gastric mucosa cells. On reaching the gastric mucosa Helicobacter pylori adheres to epithelial cells and bacterial antigens, chemotaxins and other components are liberated. Helicobacter pylori antigens are presented to immunate B lymphocytes, which interact with T-helper lymphocytes to become mature IgA-, IgD-, IgE-, IgG and Ig-M producing plasma cells. IgA dimers of secretory IgA are secreted through the gastric epithelium. IgE antibodies bind to basophils, which mature to histamine-producing mast cells. Histamine activates the acid production in the stomach and contributes to the chronic inflammation and tissue destruction. In addition, T lymphocytes are possible activated by Helicobacter pylori and contribute to the chronic inflammation.

Original languageEnglish
Pages (from-to)329-337
Number of pages9
JournalActa Physiologica Hungarica
Volume87
Issue number4
Publication statusPublished - 2000

Fingerprint

Helicobacter Infections
Helicobacter pylori
Stomach
Mucus
Gastric Mucosa
Immunoglobulin A
Immunoglobulin E
Histamine
Inflammation
Bacteria
Bacterial Antigens
Immunoglobulin D
Secretory Immunoglobulin A
Lactoferrin
Basophils
Chemotactic Factors
Helper-Inducer T-Lymphocytes
Plasma Cells
Mast Cells
B-Lymphocytes

Keywords

  • Chronic inflammation
  • Gastric epithelial cells
  • Helicobacter pylori
  • Secretory immunglobulins

ASJC Scopus subject areas

  • Physiology

Cite this

Immunological aspects of Helicobacter pylori infection. / Rácz, I.

In: Acta Physiologica Hungarica, Vol. 87, No. 4, 2000, p. 329-337.

Research output: Contribution to journalArticle

@article{0e66319f3afb4523bf26d15b45a46160,
title = "Immunological aspects of Helicobacter pylori infection",
abstract = "Host defence against Helicobacter pylori infection is a complex system of both specific and non-specific reactions. Among the non-specific defense mechanisms acting on bacteria before they reach the mucus layer in the stomach are digestive enzymes, lyzozyme, lactoferrin and other components with antimicrobal activity. The mucus layer is the final non-specific barrier against the bacteria reaching the gastric mucosa cells. On reaching the gastric mucosa Helicobacter pylori adheres to epithelial cells and bacterial antigens, chemotaxins and other components are liberated. Helicobacter pylori antigens are presented to immunate B lymphocytes, which interact with T-helper lymphocytes to become mature IgA-, IgD-, IgE-, IgG and Ig-M producing plasma cells. IgA dimers of secretory IgA are secreted through the gastric epithelium. IgE antibodies bind to basophils, which mature to histamine-producing mast cells. Histamine activates the acid production in the stomach and contributes to the chronic inflammation and tissue destruction. In addition, T lymphocytes are possible activated by Helicobacter pylori and contribute to the chronic inflammation.",
keywords = "Chronic inflammation, Gastric epithelial cells, Helicobacter pylori, Secretory immunglobulins",
author = "I. R{\'a}cz",
year = "2000",
language = "English",
volume = "87",
pages = "329--337",
journal = "Physiology International",
issn = "2498-602X",
publisher = "Akademiai Kiado",
number = "4",

}

TY - JOUR

T1 - Immunological aspects of Helicobacter pylori infection

AU - Rácz, I.

PY - 2000

Y1 - 2000

N2 - Host defence against Helicobacter pylori infection is a complex system of both specific and non-specific reactions. Among the non-specific defense mechanisms acting on bacteria before they reach the mucus layer in the stomach are digestive enzymes, lyzozyme, lactoferrin and other components with antimicrobal activity. The mucus layer is the final non-specific barrier against the bacteria reaching the gastric mucosa cells. On reaching the gastric mucosa Helicobacter pylori adheres to epithelial cells and bacterial antigens, chemotaxins and other components are liberated. Helicobacter pylori antigens are presented to immunate B lymphocytes, which interact with T-helper lymphocytes to become mature IgA-, IgD-, IgE-, IgG and Ig-M producing plasma cells. IgA dimers of secretory IgA are secreted through the gastric epithelium. IgE antibodies bind to basophils, which mature to histamine-producing mast cells. Histamine activates the acid production in the stomach and contributes to the chronic inflammation and tissue destruction. In addition, T lymphocytes are possible activated by Helicobacter pylori and contribute to the chronic inflammation.

AB - Host defence against Helicobacter pylori infection is a complex system of both specific and non-specific reactions. Among the non-specific defense mechanisms acting on bacteria before they reach the mucus layer in the stomach are digestive enzymes, lyzozyme, lactoferrin and other components with antimicrobal activity. The mucus layer is the final non-specific barrier against the bacteria reaching the gastric mucosa cells. On reaching the gastric mucosa Helicobacter pylori adheres to epithelial cells and bacterial antigens, chemotaxins and other components are liberated. Helicobacter pylori antigens are presented to immunate B lymphocytes, which interact with T-helper lymphocytes to become mature IgA-, IgD-, IgE-, IgG and Ig-M producing plasma cells. IgA dimers of secretory IgA are secreted through the gastric epithelium. IgE antibodies bind to basophils, which mature to histamine-producing mast cells. Histamine activates the acid production in the stomach and contributes to the chronic inflammation and tissue destruction. In addition, T lymphocytes are possible activated by Helicobacter pylori and contribute to the chronic inflammation.

KW - Chronic inflammation

KW - Gastric epithelial cells

KW - Helicobacter pylori

KW - Secretory immunglobulins

UR - http://www.scopus.com/inward/record.url?scp=0034571178&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034571178&partnerID=8YFLogxK

M3 - Article

C2 - 11732887

AN - SCOPUS:0034571178

VL - 87

SP - 329

EP - 337

JO - Physiology International

JF - Physiology International

SN - 2498-602X

IS - 4

ER -