The immunobiology of Helicobacter pylori gastritis

R. M. Genta

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Helicobacter pylori is the major causative agent of chronic gastritis. It is associated with duodenal and gastric ulcer and with the majority of primary gastric B-cell lymphomas; furthermore, there is a strong epidemiological association with gastric cancer. One intriguing aspect of this infection is the ability of H pylori to persist despite the vast array of host immune responses. This article reviews what is known about the immune responses against H pylori, emphasizing what is generally accepted and applicable while highlighting areas of controversy. The first section delineates the genesis of the inflammatory responses, which initiate with the production of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (11)-1, IL-6, and IL-8 and continue with the recruitment of neutrophilic polymorphonuclear cell's, lymphocytes, plasma cells, macrophages and eosinophils, and later with the development and recruitment of specifically committed cells (lymphocytes sensitized to H pylori antigens and B cells producing immunoglobulin (Ig)A, IgG, and possibly IgE antibodies against a variety of H pylori surface and flagellar proteins as well as bacterial toxins). The second part of the article focuses on the development of lymphoid follicles in the gastric mucosa, a phenomenon that for the first time links an immune response (the recruitment of mucosa-associated lymphoid tissue [MALT] to the gastric mucosa in response to H pylori infection) with the development of a neoplastic growth (the development of gastric MALT lymphomas). The local and systemic antibody responses are discussed in the light of their potential application in the development of diagnostic tests and vaccines. Particular emphasis is placed on the controversies surrounding the significance of antibodies directed against a 120 to 140 kDa protein apparently associated with more 'aggressive' (sometimes also called 'ulcerogenic' or 'pathogenic') strains of H pylori.

Original languageEnglish (US)
Pages (from-to)2-11
Number of pages10
JournalSeminars in Gastrointestinal Disease
Volume8
Issue number1
StatePublished - 1997

Fingerprint

Pylorus
Gastritis
Helicobacter pylori
Gastric Mucosa
Lymphocytes
Interleukin-11
Bacterial Toxins
Marginal Zone B-Cell Lymphoma
Antibodies
B-Cell Lymphoma
Lymphoid Tissue
Stomach Ulcer
Duodenal Ulcer
Infection
Plasma Cells
Interleukin-8
Interleukin-1
Growth and Development
Routine Diagnostic Tests
Eosinophils

ASJC Scopus subject areas

  • Gastroenterology

Cite this

The immunobiology of Helicobacter pylori gastritis. / Genta, R. M.

In: Seminars in Gastrointestinal Disease, Vol. 8, No. 1, 1997, p. 2-11.

Research output: Contribution to journalArticle

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