How Does Helicobacter pylori Cause Mucosal Damage? The Inflammatory Response

doi:10.1016/S0016-5085(97)80009-1

Gastroenterology

Volume 113, Issue 6, Supplement, December 1997, Pages S35-S42

https://doi.org/10.1016/S0016-5085(97)80009-1 Get rights and content

Abstract

The role for Helicobacter pylori in the pathogenesis of disease provides the conundrum that only a subset of subjects infected with H. pylori will ever develop peptic ulcer or gastric cancer. Thus, variation in strain as well as environmental or host factors converge in the gastroduodenal milieu and control the final outcome of infection. The host immune and inflammatory response is emerging as an important element in the pathogenesis of these gastric diseases. The ideal host response provides protection to clear an infection without causing excessive amounts of inflammation that could compromise the integrity and function of host cells. This review will cover four main questions: (1) What are the mucosal immune/inflammatory responses that confer protection without damaging the host? (2) How do the gastric immune responses during infection with H. pylori differ from this ideal scenario? (3) Do these responses contribute to autoimmune-mediated damage to gastric tissue? (4) Can immunomodulation through vaccination enhance protective, nondestructive responses that prevent or treat infection or, at least, attenuate inflammation?

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It has been suggested that Helicobacter pylori as a factor of chronic inflammation in the stomach disrupts the balance between gastric epithelial cell proliferation and apoptosis leading to the development of gastric cancer [1–4].
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How Does Helicobacter pylori Cause Mucosal Damage? The Inflammatory Response

Abstract

Vaccine

Gastroenterology

Zentralbl Bakteriol

Immunol Today

Lancet

Gastroenterology

Gastroenterology

Gastroenterology

Gastroenterology

Gastroenterology

J Biol Chem

Lancet

Gastroenterology

Oral immunization: turning fantasy into reality

Int Arch Allergy Immunol

Identification of novel lymphoid tissues in murine intestinal mucosa where clusters of c-kit+ IL-7R+ Thy1+ lymphohemopoietic progenitors develop

J Exp Med

A distinct array of proinflammatory cytokines is expressed in human colon epithelial cells in response to bacterial invasion

J Clin Invest

Novel Pseudomonas product stimulates interleukin-8 production in airway epithelial cells in vitro

J Clin Invest

Helper T cell subsets for immunoglobulin A responses: oral immunization with tetanus toxoid and cholera toxin as adjuvant selectively induces Th2 cells in mucosa associated tissues

J Exp Med

Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis

Science

Mucosal tumour necrosis factor a and interleukin-6 in patients with Helicobacter pylori associated gastritis

Gut

Mucosal tumor necrosis factor-alpha, interleukin-1 beta and interleukin-8 production in patients with Helicobacter pylori

Scand J Gastroenterol

Immunological aspects

Curr Opin Gastroenterol

Interferon gamma and interleukin 4 secreting cells in the gastric antrum in Helicobacter pylori positive and negative gastritis

Gut

Epithelial expression of HLA, secretory component (poly-Ig receptor) and adhesion molecules in the human alimentary tract

Ann NY Acad Sci

Overview of the immune response to H. pylori

Pathophysiology of Helicobacter pylori infection

Scand J Gastroenterol

Helicobacterassociated gastritis in SCID mice

Infect Immun

Effects of neutrophil-derived oxidants on intestinal permeability, electrolyte transport, and epithelial cell viability

Inflammation

Relationship between infection load of Helicobacter pylori and reactive oxygen metabolite production in antral mucosa

Scand J Gastroenterol

Neutrophil migration across a cultured epithelial monolayer elicits a biphasic resistance response representing sequential effects on transcellular and paracellular pathways

J Cell Biol

Characterization of a Helicobacter pylori neutrophil-activating protein

Infect Immun

Identification of novel lymphoid tissues in murine intestinal mucosa where clusters of c-kit⁺ IL-7R⁺ Thy1⁺ lymphohemopoietic progenitors develop